The study emphasizes that metabolic dysfunction can lead to a cascade of health complications, particularly for individuals suffering from T2DM. As obesity rates climb and lifestyle habits shift towards less activity and poorer diet, the incidence of MASLD is predicted to rise dramatically. This presents considerable public health challenges, especially in developing countries like Tanzania, where limited healthcare resources complicate early detection and management.

In Tanzania, researchers focused on a cohort of patients diagnosed with T2DM to ascertain the prevalence of MASLD within this vulnerable population. Remarkably, findings indicated that a substantial proportion of the study participants harbored indications of liver steatosis, up to 30%, underscoring the urgent need for awareness and diagnostic efforts among healthcare professionals in the region. Early detection of such liver abnormalities can lead to timely interventions that might significantly alter disease progression outcomes.

The study goes on to reveal several predictors of MASLD in the patient cohort. Among these, obesity stands out as a significant risk factor. Individuals with body mass index (BMI) categorized as overweight or obese were found to face a markedly higher risk of developing liver disease. This highlights a crucial target area for intervention, as weight management strategies could play a powerful role in mitigating the risks associated with MASLD.

Another important finding from the research is the impact of lifestyle factors, including dietary habits and physical inactivity. Patients who reported high caloric intake or consumed diets rich in sugars and saturated fats were more likely to exhibit symptoms of metabolic dysfunction. Conversely, those who engaged in regular physical activity had a reduced prevalence of MASLD, reinforcing the importance of lifestyle modification in disease prevention.

Furthermore, metabolic syndrome components such as hypertension and dyslipidemia were noted as concurrent conditions in many patients with MASLD. This interrelationship suggests that managing these cardiovascular risk factors is crucial not only for improving overall health but also for addressing liver health in diabetic patients. The multifaceted nature of these syndromes emphasizes the need for an integrated approach to treatment, catering to the various facets of patients’ health.

The implications of these findings reach far beyond Tanzania, as they mirror global trends. With rising diabetes rates worldwide, the this research serves as a clarion call for health initiatives tailored to prevent and manage MASLD. Additionally, it indicates that greater education and training for healthcare providers are essential in recognizing and addressing the symptoms of liver dysfunction early on.

Moreover, public health campaigns focusing on lifestyle modification and preventive health can equip populations with the necessary tools to combat the dual challenges of diabetes and liver disease. In doing so, societies can aspire to diminish the burden of chronic diseases that threaten sustainable healthcare systems.

In conclusion, the study sheds light on the dire need for awareness and intervention regarding MASLD in populations with T2DM. As diabetes continues to be a growing concern across the globe, understanding the associated risks of liver disease becomes increasingly essential. Tunisia’s pioneering research serves as a critical resource for targeted, evidence-based strategies that can improve patient outcomes on both a local and global scale.

This investigation into MASLD among diabetic patients not only underscores the relationship between these conditions but also emphasizes the vital importance of maintaining optimal health through individual lifestyle choices and broader public health interventions. With continued research and collaboration, we can foster a future where such diseases are effectively managed or even eliminated through strategic efforts grounded in science and compassion.

The study reflects not only the immediate health challenges within Tanzania but also reinforces the need for a collective response to chronic diseases that are prevalent in various regions of the world. The partnership between patients, healthcare professionals, and public health authorities is paramount in leading the charge against the rising tide of metabolic diseases that threaten the health of future generations.

Subject of Research: Metabolic dysfunction-associated steatotic liver disease and its relationship with type 2 diabetes mellitus in Tanzania.

Article Title: Metabolic dysfunction-associated steatotic liver disease in patients with type 2 diabetes mellitus in Tanzania: prevalence and predictors.

Article References:

Malindisa, E., Kafumu, I., Rweyendera, A. et al. Metabolic dysfunction-associated steatotic liver disease in patients with type 2 diabetes mellitus in Tanzania: prevalence and predictors.
BMC Endocr Disord (2026). https://doi.org/10.1186/s12902-026-02179-0

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02179-0

Keywords: metabolic syndrome, type 2 diabetes mellitus, liver disease, prevalence, public health, Tanzania.

Hepatic stellate cells (HSCs), traditionally regarded as the primary cells responsible for liver fibrosis development, have now emerged as pivotal players in the transition from liver injury to cirrhosis and ultimately to liver cancer. The researchers discovered that EMP1+, a specific marker of activated hepatic stellate cells, significantly contributes to the fibrogenic response within the liver. This activation can result from a myriad of stimuli, including chronic viral hepatitis, alcohol consumption, and metabolic disorders. The intricate interplay of these factors sets the stage for the development of fibrosis, which becomes a precursor to HCC in susceptible individuals.

The significance of EMP1+ hepatic stellate cells emerges not only from their role in fibrosis but also in their capacity to influence the tumor microenvironment. The study demonstrated that these cells secrete various cytokines and growth factors that promote tumor growth and metastasis. The findings indicate that EMP1+ HSCs are not merely passive observers in the pathological landscape of the liver; rather, they actively contribute to creating a pro-tumorigenic environment, thereby facilitating the transition from non-cancerous liver disease to malignant tumors.

In a comprehensive analysis, the researchers employed advanced imaging techniques to visualize EMP1+ hepatic stellate cells within liver tissue samples from both animal models and human patients. By correlating these findings with clinical data, the team was able to establish a relationship between the abundance of EMP1+ cells and the severity of hepatic fibrosis. These results are particularly relevant as they suggest that the quantification of these cells may serve as a valuable prognostic biomarker, enabling clinicians to better predict the progression of liver disease towards HCC.

Moreover, the impact of EMP1+ hepatic stellate cells extends beyond their role in fibrosis and cancer progression; the study also identified their involvement in immune modulation within the liver. By altering the local immune context, these cells can skew the immune response, potentially allowing tumor cells to evade immune surveillance. This immune evasion is a hallmark of cancer biology and presents significant challenges for therapeutic interventions aimed at reinstating effective anti-tumor immunity.

In the quest for targeted therapies, understanding the molecular pathways activated within EMP1+ hepatic stellate cells could unveil innovative treatment strategies. The research highlights several key signaling pathways, including TGF-β and Hedgehog, which have previously been implicated in liver fibrosis and cancer progression. By inhibiting these pathways, it may be possible to disrupt the tumor-promoting activities of EMP1+ HSCs, thereby addressing both fibrosis and its oncogenic sequelae in a dual-targeted approach.

Additionally, the study’s findings emphasize the importance of early detection and monitoring of liver fibrosis. Given that HCC often develops silently over many years, identifying patients at risk through the assessment of EMP1+ hepatic stellate cells could lead to earlier interventions and potentially save lives. Implementing routine screenings and profiling patients for biomarkers associated with fibrogenesis may significantly reduce the burden of advanced liver disease.

Furthermore, the researchers note the potential for EMP1+ hepatic stellate cells to serve as a therapeutic target for novel drug development. As our understanding of liver pathology deepens, the prospect of developing drugs that specifically modulate the activity or recruitment of these cells opens exciting avenues for clinical research. Targeting the cellular mechanisms that drive hepatic fibrosis and cancer progression could revolutionize treatment approaches, offering hope to patients with limited treatment options.

The implications of this study extend beyond the realm of experimental findings; they underscore the critical need for interdisciplinary collaboration in addressing the multifaceted challenges posed by liver diseases. By integrating insights from molecular biology, immunology, and clinical research, scientists and clinicians can forge a comprehensive understanding of the pathways that govern the progression from fibrosis to HCC. Such collaborations will ultimately enhance patient care and outcomes in the growing population of individuals affected by liver diseases.

As the global prevalence of liver diseases continues to rise, driven in part by the increasing rates of obesity, viral hepatitis, and alcohol-related liver injury, the urgency for effective therapeutic strategies has never been more critical. The breakthrough findings from You, Huang, and Jiang could serve as a catalyst for renewed interest in the research surrounding hepatic stellate cells and their roles in liver pathology. By shifting the focus toward EMP1+ HSCs, researchers can open new frontiers in diagnosis, treatment, and patient prognosis.

In conclusion, the study highlights EMP1+ hepatic stellate cells as key mediators in the progression of liver fibrosis to hepatocellular carcinoma. Their dual role in promoting fibrosis and facilitating tumor growth marks them as critical players in the pathology of liver disease. The findings bear significant implications for both research and clinical practice, paving the way for innovative strategies to combat liver fibrosis and HCC, ultimately aiming to improve patient outcomes in this challenging field of medicine.

Subject of Research: The role of EMP1+ hepatic stellate cells in liver fibrosis progression to hepatocellular carcinoma and their potential as prognostic markers.

Article Title: EMP1 + hepatic stellate cells drive hepatic fibrosis progression to hepatocellular carcinoma and predict prognosis.

Article References:

You, J., Huang, Y., Jiang, C. et al. EMP1 + hepatic stellate cells drive hepatic fibrosis progression to hepatocellular carcinoma and predict prognosis. J Transl Med (2025). https://doi.org/10.1186/s12967-025-07454-7

Image Credits: AI Generated

DOI: 10.1186/s12967-025-07454-7

Keywords: Hepatic stellate cells, liver fibrosis, hepatocellular carcinoma, EMP1+, tumor microenvironment, immune modulation, prognostic biomarkers, TGF-β, Hedgehog signaling.

The liver and pancreas serve as paramount organs with crucial roles in various physiological processes. The liver, performing over 500 vital functions, is responsible for detoxifying harmful substances, regulating blood sugar levels, and producing essential proteins. Simultaneously, the pancreas orchestrates the delicate balance of insulin and glucagon to manage glucose levels, manage digestion through enzyme production, and contribute to metabolic health. Understanding the nuanced innervation of these organs can potentially lead to novel therapeutic interventions for metabolic disorders and other liver and pancreatic diseases.

A major focus of the study was the application of advanced neurohistological techniques that allow for high-resolution imaging of the neural networks within the liver and pancreas. Traditional methods have often been limited by their inability to provide a comprehensive view of the three-dimensional configuration of nerve fibers. However, the use of cutting-edge imaging modalities has afforded researchers the opportunity to map these neural structures with unprecedented clarity, thereby revealing the interconnections between nerve fibers and their target cells. This not only enhances our understanding of organ function but also demonstrates how neural pathways interact to support metabolic regulation.

The research team utilized intricate 3D reconstructions of neuronal architecture to discern patterns of innervation across various regions of the liver and pancreas. By employing a combination of immunohistochemistry and high-resolution imaging techniques, they meticulously delineated the distributions of autonomic nerve fibers, including sympathetic and parasympathetic pathways. This endeavor is pivotal as it highlights not only the complexity of the nervous system but also the dynamic interplay between these two branches of the autonomic nervous system in maintaining homeostasis.

Additionally, the study emphasizes the critical role of the enteric nervous system, often referred to as the “second brain.” The enteric nervous system governs gastrointestinal function and interacts significantly with the central nervous system. Understanding its connections to the liver and pancreas opens new avenues for exploring how gut health influences metabolic processes and vice versa. The bidirectional communication between these organs may shed light on the pathophysiology of diabetes, obesity, and liver diseases, pointing researchers toward innovative therapeutic strategies.

One of the standout findings from this research is the discovery of novel nerve fiber populations that were previously overlooked in conventional studies. Through meticulous examination, the researchers identified specialized nerve fibers that appear to play a role in modulating the secretory activities of the pancreas. These findings have profound implications for our understanding of how neural inputs influence hormonal release and metabolic responses, especially in conditions like type 2 diabetes where insulin signaling is disrupted.

As metabolic diseases continue to rise globally, the insights gained from this research are particularly timely. The identification of specific neural circuits involved in metabolic regulation and pancreatic function might guide the development of targeted interventions to restore proper balance in metabolic pathways. Moreover, elucidating the neural circuits may help identify biomarkers for early diagnosis and treatment of diseases related to liver and pancreas dysfunction.

Furthermore, the implications of this research extend beyond individual health. A deeper understanding of the liver and pancreas innervation can illuminate how these organs interact within a broader physiological context, bringing insights relevant for public health strategies. As healthcare systems grapple with the growing burden of metabolic disorders, the need for comprehensive understandings of underlying biological mechanisms becomes increasingly urgent. This study provides a critical foundation for developing future health interventions.

The work by Lee et al. could also inspire further studies aimed at investigating the molecular mechanisms underlying nervous system influences on the liver and pancreas. Understanding the signaling pathways involved, and the potential for neuroprotective or regenerative therapies, could open doors for novel treatments. Researchers may discover pharmacological agents that can selectively target these neural circuits to enhance organ function, improve metabolic health, or combat diseases.

In conclusion, the groundbreaking research into the innervation of the human liver and pancreas not only resolves existing knowledge gaps but also lays the groundwork for future studies. Lee et al. have successfully combined advanced neurohistological techniques with a visionary approach to mapping intricate neural pathways. This comprehensive exploration of nerve fibers within these critical organs represents a significant step forward in biomedical research. As we delve deeper into the interconnected roles of the nervous system and metabolic regulation, the potential for transformative discoveries beckons, promising a future where precision medicine becomes a reality for treating metabolic disorders.

The implications of this study are vast, and as researchers begin to unpack the complexities revealed, we can anticipate a surge of interest in the fields of neurobiology and metabolic health. The road ahead is paved with possibilities, as the intersections between our nervous systems and organ functions continue to be illuminated by ongoing research and technological advancements. Exciting times lie ahead in the quest for new possibilities in treating and understanding human health.

The implications stretch into various domains, including the integration of this knowledge into clinical settings, potentially influencing treatment paradigms for conditions such as diabetes and fatty liver disease. It is not merely an academic exercise; these findings may considerably shift the landscape of patient care. As the research community digs deeper into the neural regulation of organ function, we can expect an evolving narrative that not only informs scientific dialogue but also translates into actionable strategies for improving patient outcomes.

In summary, the newly uncovered intricacies of human liver and pancreas innervation represent a frontier of scientific inquiry with immense potential. As Lee et al. pave the way with their findings, the ripple effects of this research are bound to foster further investigations that bridge gaps, inspire innovation, and ultimately lead to improved healthcare solutions.

Subject of Research: Human liver and pancreas innervation

Article Title: Human liver and pancreas innervation: resolving 3D neurohistological challenges and advancing insights

Article References:

Lee, CY., Hsiao, FT., Chen, CC. et al. Human liver and pancreas innervation: resolving 3D neurohistological challenges and advancing insights.
J Biomed Sci 32, 97 (2025). https://doi.org/10.1186/s12929-025-01194-y

Image Credits: AI Generated

DOI: https://doi.org/10.1186/s12929-025-01194-y

Keywords: liver, pancreas, innervation, neurohistology, metabolism, neuropathology, diabetes, research, biomedical science.

Liver cirrhosis is the end-stage manifestation of chronic liver disease, characterized by extensive hepatic fibrosis and resultant deterioration of liver function. The etiology of cirrhosis can vary, with chronic alcohol abuse, viral infections, autoimmunity, and metabolic disorders being major underlying causes. As the liver is crucial for numerous bodily functions including metabolism and detoxification, the ramifications of cirrhosis on overall health are profound and can lead to complications such as hepatic encephalopathy, portal hypertension, and increased risk of liver cancer.

In their study published in the Journal of Translational Medicine, Zheng et al. highlight the role of macrophages in liver pathology. Macrophages serve as pivotal components of the immune system, possessing the capability to polarize into different phenotypes that can either exacerbate or resolve inflammation. The dysregulation of these immune cells within the liver microenvironment is a decisive factor contributing to the progression of liver diseases, including cirrhosis. The authors suggest that by targeting macrophage regulatory mechanisms, it may be possible to modify the disease trajectory significantly.

Targeting macrophages as a therapeutic strategy is particularly compelling given their prominence in mediating inflammatory responses within the liver. Their plasticity allows them to adopt pro-inflammatory or anti-inflammatory states depending on the local microenvironment. In patients with liver cirrhosis, it is often observed that there is a shift towards a pro-inflammatory macrophage phenotype. This perpetuates a cycle of inflammation and further fibrogenesis, worsening the condition. Therefore, reprogramming macrophages to assume a protective role could have transformative effects on patient outcomes.

Zheng and his team delve into several potential avenues for manipulating macrophage behavior. One innovative approach involves the use of small-molecule compounds that can effectively reorient macrophages towards an anti-inflammatory state. The transition from a M1 (pro-inflammatory) to a M2 (anti-inflammatory) phenotype represents a potential therapeutic goal, fostering an environment conducive to tissue repair and regeneration within the damaged liver.

In addition to pharmacological interventions, the study also explores the potential of gene therapy as a means to influence macrophage function. By employing techniques such as CRISPR-Cas9 to modify genes responsible for macrophage polarization, researchers hope to establish more durable changes in macrophage behavior that would promote healing and mitigate fibrosis. Although challenges remain in delivering such therapies effectively to the liver, the results from preliminary studies show encouraging promise.

Zheng et al. further emphasize the importance of the liver’s unique microenvironment and the role it plays in macrophage activation. Notably, the presence of various stimuli, such as cytokines and growth factors, shapes how macrophages respond to liver injury and influences whether they contribute positively or negatively to the healing process. The identification of specific signaling pathways involved in macrophage activation represents a critical step in devising strategies to selectively inhibit detrimental macrophage responses while enhancing positively reparative actions.

The implications of this research extend beyond liver cirrhosis, potentially informing the treatment of other fibrotic diseases. Similar macrophage-driven inflammatory processes are also observed in conditions affecting the lungs, kidneys, and heart, suggesting that insights gained from this study may apply widely across various organs and conditions. The ability to leverage macrophage biology could revolutionize our approach to not just cirrhosis, but a broad array of inflammatory diseases.

As this work progresses, researchers are faced with further challenges, including the need for extensive clinical trials to assess the safety and efficacy of these novel interventions. While preclinical data is promising, translating these findings into real-world treatments demands meticulous consideration of numerous factors, including patient heterogeneity, the stage of disease, and potential side effects associated with macrophage modulation therapies.

The urgency of advancing liver cirrhosis treatments cannot be overstated. The chronic nature of this disease, coupled with its complications, necessitates innovative strategies that differ markedly from traditional approaches focused primarily on managing symptoms. By redirecting focus towards the immune system’s intricacies, particularly macrophages, Zheng and his team could be laying the groundwork for a new paradigm in addressing liver cirrhosis that emphasizes restoration of normal immune function over mere symptom alleviation.

Insights from this study also align with an increasing interest in personalized medicine. By understanding the unique macrophage profiles present in different patients, it may be possible to develop tailored therapies that reflect individual disease pathways and immune profiles. This could improve treatment outcomes and ultimately lead to more sustainable long-term management strategies for patients afflicted by liver cirrhosis.

In conclusion, the research conducted by Zheng et al. provides an exciting glimpse into the future of liver cirrhosis treatment. By targeting macrophage regulatory mechanisms, they pave the way for potentially innovative therapies that can shift the narrative of this debilitating disease from one of inevitability to one of hope and recovery. As the scientific community builds upon these findings, the goal will be to translate laboratory discoveries into tangible clinical solutions that improve quality of life and outcomes for those facing the challenges of liver cirrhosis. The journey ahead is undoubtedly complex, but the promise held in these new approaches signals a brighter future for liver disease management.

Subject of Research: Liver cirrhosis and macrophage regulatory mechanisms

Article Title: New perspectives in the treatment of liver cirrhosis: targeting macrophage regulatory mechanisms.

Article References:

Zheng, S., Li, S., Wang, Q. et al. New perspectives in the treatment of liver cirrhosis: targeting macrophage regulatory mechanisms.
J Transl Med 23, 1201 (2025). https://doi.org/10.1186/s12967-025-07239-y

Image Credits: AI Generated

DOI: 10.1186/s12967-025-07239-y

Keywords: Liver cirrhosis, macrophages, immunotherapy, fibrosis, inflammation, personalized medicine, regenerative medicine

Ribosome biogenesis is a multifaceted and highly orchestrated process that starts in the nucleolus, a specialized subnuclear structure, where ribosomal RNA (rRNA) is transcribed primarily by RNA polymerase I. The process entails the synthesis and processing of precursor rRNA transcripts, coordinated incorporation of ribosomal proteins, and assistance from a large cohort of assembly factors. Once these components are assembled into pre-ribosomal subunits, they are exported to the cytoplasm for maturation into functional ribosomes. This entire biogenetic pathway ensures that the cell maintains a robust protein production capacity indispensable for liver cells, which must frequently regenerate and respond to metabolic demands.

The liver’s phenomenal capacity to regenerate after injury is intimately tied to ribosome biogenesis. Hepatocytes ramp up protein synthesis machinery to facilitate replication and repair, a process heavily reliant on efficient ribosome production. Any disruption in ribosome assembly impairs this regenerative capability, predisposing liver tissue to damage and functional decline. This mechanistic insight underscores why ribosome biogenesis is central not only to normal liver physiology but also to the pathology of liver diseases triggered by injury or infection.

In the context of hepatitis C virus (HCV) infection, ribosomes assume an additional, more sinister role. HCV exploits the host’s translational machinery for viral protein synthesis and replication. The viral lifecycle is tightly dependent on the host’s ribosomal function, rendering ribosome biogenesis a double-edged sword in infection scenarios. Notably, therapeutic strategies targeting components of ribosome synthesis or function emerge as promising candidates to hinder viral propagation, representing a novel front in antiviral drug development.

Nonalcoholic fatty liver disease (NAFLD), a metabolic disorder characterized by excessive fat accumulation within hepatocytes, has also been linked to the modulation of ribosomal activity. Enhanced ribosome biogenesis correlates with increased lipogenesis, the process by which fatty acids and triglycerides are synthesized. This suggests that ribosomes are actively involved in metabolic reprogramming that underlies NAFLD progression. By targeting ribosomal pathways, there may be potential to modulate metabolic derangements and attenuate disease severity.

Chronic liver diseases such as fibrosis and cirrhosis develop following persistent injuries that promote excessive extracellular matrix production and scarring. At the molecular level, activated hepatic stellate cells (HSCs) drive this fibrogenic response, and this activation is closely linked to aberrant ribosome biogenesis. Overactive ribosomal machinery in HSCs can fuel their proliferation and secretion of matrix components, exacerbating fibrosis. A deeper understanding of ribosome assembly within these cells offers prospects for interrupting the fibrotic cascade at its source.

Hepatocellular carcinoma (HCC), the most common form of liver cancer, stands out as a disease profoundly influenced by dysregulated ribosome biogenesis. Tumor cells frequently exhibit elevated ribosome production to meet their increased protein synthesis demands, enabling rapid growth and proliferation. Elevated rRNA transcription, ribosomal protein overexpression, and alterations in assembly factors collectively contribute to oncogenesis. Importantly, this overdrive in ribosome biogenesis represents a vulnerability that can be exploited therapeutically.

Pharmacological inhibitors designed to disrupt ribosome biogenesis are in various stages of development and testing. One notable compound, CX-5461, targets RNA polymerase I-mediated rRNA transcription, effectively dampening ribosome production. Preclinical studies demonstrate that CX-5461 can induce nucleolar stress and apoptosis selectively in cancer cells, highlighting its potential as a liver cancer therapeutic. These agents exemplify a shift toward targeting the tumor’s protein synthesis platform rather than its genetic mutations alone.

Beyond monotherapy, there is optimism surrounding the combination of ribosome-targeting drugs with standard chemotherapy regimens. Such combinations could enhance treatment efficacy by simultaneously crippling cancer cells’ protein production capability and conventional cytotoxic pathways. This multifaceted attack might overcome therapeutic resistance often encountered in advanced liver cancers, improving patient outcomes and survival rates.

The molecular pathways linking ribosome biogenesis to liver pathology are complex, involving numerous signaling networks and checkpoints. These include regulatory feedback loops ensuring cellular homeostasis and stress responses that either augment or suppress ribosome assembly under pathological conditions. Elucidating these pathways furnishes a blueprint for designing highly specific interventions that minimize off-target effects and toxicity.

The implications of this review extend beyond liver diseases, inviting a broader research interest into ribosome biogenesis as a central hub in multiple disease states. The approach of manipulating the cell’s translational apparatus challenges traditional paradigms and exemplifies precision medicine at a subcellular level. By honing in on the molecular underpinnings of ribosome production, scientists are pioneering novel, targeted therapies that promise to revolutionize how we treat liver ailments.

In conclusion, ribosome biogenesis stands at the crossroads of liver health and disease, from regeneration following injury to the pathophysiology of viral infections, metabolic disorders, fibrosis, and cancer. This review underscores not only the biological significance of ribosome assembly but also its therapeutic potential, marking it as a vital focus in hepatology research. Harnessing our understanding of this process could usher in a new era of effective, targeted treatment strategies for some of the most challenging liver diseases.

Subject of Research: Ribosome biogenesis and its role in liver diseases

Article Title: Ribosome biogenesis: A central player in liver diseases

News Publication Date: 2025

References: Wei Luo, Jing Zhou, Yongmin Yan, Xuezhong Xu, Ribosome biogenesis: A central player in liver diseases, Genes & Diseases, Volume 12, Issue 5, 2025, 101512

Image Credits: Genes & Diseases

Keywords: Cancer genetics, Ribosome biogenesis, Liver regeneration, Hepatitis C virus, Nonalcoholic fatty liver disease, Liver fibrosis, Cirrhosis, Hepatocellular carcinoma, CX-5461, RNA polymerase I inhibitors