The scale of the microbial contribution is difficult to overstate. The intestinal microbiota contains a gene pool approximately 150 times larger than the human genome, dominated by four major phyla: Bacteroides, Firmicutes, Proteobacteria and Actinomycetes. The ratio of Firmicutes to Bacteroidetes has emerged as a recurring biomarker of microbial imbalance, or dysbiosis, across conditions ranging from obesity to hypertension. In health, the community operates in eubiosis, a balanced state in which microbes signal to host cells, train the immune system, protect against pathogens and regulate nutrient metabolism. When that balance collapses, the review finds, the consequences ripple far beyond the gut wall.

Technically, the microbiota’s influence flows through a small set of chemically well-defined metabolites. Fermentation of undigested carbohydrates by saccharolytic bacteria such as Bifidobacteria, Bacteroides, Faecalibacterium and Roseburia yields the short-chain fatty acids acetate, propionate and butyrate. These molecules bind G-protein-coupled receptors including GPR41, GPR43 and GPR109A on enteroendocrine and immune cells, triggering cAMP/PKA signaling that drives secretion of the satiety hormones GLP-1 and PYY, and inhibiting histone deacetylases to promote anti-inflammatory regulatory T cells. Bile acids, deconjugated in the colon by organisms such as Bacteroides intestinalis, signal through the nuclear receptor FXR and the membrane receptor TGR5 to regulate lipid metabolism and glucose homeostasis. Meanwhile, microbial metabolism of choline, carnitine and betaine generates trimethylamine, which the liver converts to trimethylamine N-oxide, or TMAO, a compound now firmly linked to cardiovascular risk.

The cardiovascular findings are among the most striking. Hypertensive patients show significant decreases in microbial diversity and richness and a markedly elevated Firmicutes-to-Bacteroidetes ratio, and a meta-analysis of eighteen observational studies found blood TMAO concentrations associated with hypertension risk in a dose-dependent manner. Mechanistically, TMAO activates the PERK unfolded-protein response in endothelial cells, provoking NF-κB-mediated inflammation and vascular dysfunction, while in macrophages it drives foam cell formation through CD36 upregulation. Animal experiments reinforce causality: transplanting stool from hypertensive patients into germ-free mice raises blood pressure, and antibiotic-mediated restoration of the Bacteroidetes-to-Firmicutes ratio relieves hypertension in rats. Microbial hydrogen sulfide adds another layer, since deficiency of this vasorelaxant gas precedes the onset of high blood pressure in spontaneously hypertensive rats.

Atherosclerosis tells a parallel story. Bacterial DNA has been recovered from atherosclerotic plaques, indicating that microbes or their products can reach the vessel wall, and a metagenome-wide association study found Enterobacter aerogenes significantly enriched in patients with atherosclerosis. Dysbiosis increases intestinal permeability, allowing lipopolysaccharide to enter the circulation and fuel vascular inflammation. Elevated TMAO accelerates macrophage-to-foam-cell conversion, impairs endothelial function and promotes platelet reactivity and thrombosis, while a second microbial metabolite, phenylacetylglutamine, enhances clotting through adrenergic G-protein-coupled receptors. Counterbalancing these harmful pathways, bile acids activate FXR to suppress inflammatory cytokine expression in monocytes and macrophages, and short-chain fatty acids promote vasorelaxation through cAMP-dependent signaling in the vascular endothelium.

The gut-brain axis occupies perhaps the most provocative territory in the review. In Parkinson’s disease, patients consistently show depletion of butyrate-producing genera such as Prevotella, Faecalibacterium and Butyricicella alongside expansions of Bifidobacteria and Enterococcus. Reduced short-chain fatty acid and ghrelin signaling appears to promote alpha-synuclein aggregation and overactivation of microglia, the brain’s resident immune cells. In a landmark germ-free mouse experiment, fecal microbiota transplanted from Parkinson’s patients worsened alpha-synuclein-driven motor deficits more than transplants from healthy donors, providing some of the strongest causal evidence that gut microbes can shape neurodegeneration. Alzheimer’s disease follows a similar logic: dysbiosis elevates pro-inflammatory taxa such as Escherichia and Shigella, and accumulation of microbial-derived phenylalanine and isoleucine expands pro-inflammatory Th1 cells that inflame the central nervous system.

Experimental interventions in Alzheimer’s models are particularly encouraging. APPPS1 mice raised germ-free show markedly reduced beta-amyloid deposition and microglial activation compared with conventionally raised animals, and transferring healthy microbiota into Alzheimer’s model mice improves amyloid and tau pathology, cognitive performance and glial reactivity. The prebiotic R13 has been shown to restrain amyloid aggregation in the gastrointestinal tract by modulating the C/EBPβ-AEP pathway, while the drug sodium oligomannate, or GV-971, remodels gut flora to prevent peripheral amino acid buildup and reduce neuroinflammation. The authors caution, however, that most human studies in Parkinson’s and Alzheimer’s are cross-sectional, confounded by medication such as levodopa, and marked by inconsistent findings across cohorts, so longitudinal and standardized studies remain essential.

Metabolic disease occupies the largest share of the evidence. In obesity, the microbiota of affected individuals shows reduced diversity with losses of Akkermansia muciniphila, Bacteroides and Faecalibacterium prausnitzii, and germ-free mice receiving obese-donor microbiota gain more fat than those receiving lean-donor communities. Short-chain fatty acids counter obesity through two routes: stimulating GLP-1 and PYY release to suppress appetite, and upregulating thermogenic and lipid-oxidation proteins including PPARγ, PGC1α, UCP1 and CPT-1. In diabetes, both type 1 and type 2 forms are associated with diminished microbial diversity, and microbiota-derived metabolites such as lipopolysaccharide and flagellin disrupt epithelial tight junctions and fuel insulin resistance. Non-alcoholic fatty liver disease completes the picture through the gut-liver axis, in which increased intestinal permeability permits endotoxin and even microbially produced endogenous ethanol to reach the liver, while butyrate activates the AMPK pathway to curb hepatic lipogenesis.

On the gastrointestinal front, inflammatory bowel disease features a characteristic collapse of Firmicutes and expansion of Proteobacteria, with fungal overgrowth also documented in Crohn’s disease, and transfer of dysbiotic microbes into germ-free mice reproduces colitis. In colorectal cancer, organisms such as Peptostreptococcus anaerobius and Fusobacterium nucleatum activate oncogenic signaling and suppress anti-tumor immunity, while microbial gallic acid can even flip mutant p53 between tumor-suppressive and cancer-promoting behavior depending on gut location. The review closes with a therapeutic roadmap: personalized probiotics guided by metagenomic sequencing, polyphenol- and fiber-rich diets to boost short-chain fatty acid production, narrow-spectrum antimicrobials that spare beneficial taxa, and fecal microbiota transplantation, which already cures recurrent Clostridium difficile infection and is being explored for obesity, inflammatory bowel disease and metabolic syndrome. The authors argue that integrating bioinformatics, organoid models and artificial intelligence will be the key to translating this microbial science from correlation into clinical practice.

Beyond the disease-specific findings, the review underscores how malleable the gut ecosystem is across a human lifetime. Composition shifts from birth through aging, and population studies consistently identify diet, geography, systemic illness and pharmaceutical exposure as dominant determinants of which taxa flourish. Antibiotic overuse emerges as a particular concern, since broad-spectrum agents can destabilize the eubiotic equilibrium and predispose the host to systemic disease, whereas a nutritious diet rich in fermentable substrates sustains communities that benefit the host.

The metabolic versatility of the resident microbes is central to this story. Colon-dwelling organisms preferentially consume carbohydrates that escape digestion in the upper tract, and when those substrates run short, bacteria switch to alternative energy sources that generate potentially harmful metabolites. This substrate-dependence explains why dietary pattern, not merely caloric intake, shapes the chemical signals reaching host tissues. The archaeon Methanobrevibacter smithii illustrates the ecosystem’s complexity: by converting hydrogen produced through bacterial fermentation into methane, it fine-tunes the fermentation environment in ways that influence overall energy harvest.

Microbes also participate in processing compounds the host cannot handle alone, including xenobiotics and drugs, a capacity with direct pharmacological implications. The review notes that microbial enzymes can alter drug metabolism, which may partly explain inter-individual variation in therapeutic response and adverse effects, an area the authors suggest deserves deeper integration into personalized medicine.

Methodologically, the field has had to overcome substantial obstacles. Early estimates of intestinal species richness were undercounts, driven by the difficulty of culturing many obligate anaerobes outside the body. Molecular and metagenomic approaches have since revealed the true diversity, and the authors argue that combining bioinformatics with organoid systems and machine learning will be essential to move from associative observations toward mechanistic, predictive models of microbe-host interaction.

On translation, the review strikes a measured tone. Fecal microbiota transplantation already stands as the clearest clinical success, effectively curing recurrent Clostridium difficile infection, while narrower applications for metabolic syndrome and inflammatory bowel disease remain under investigation. Personalized probiotics selected through sequencing, prebiotic fibers that feed beneficial saccharolytic taxa, polyphenol-rich diets, and narrow-spectrum antimicrobials designed to spare commensals together form a therapeutic toolkit that the authors believe could eventually shift clinical practice from treating dysbiosis after it appears toward maintaining eubiosis preventively, provided that rigorous longitudinal human studies validate the causal pathways suggested by animal work.

Subject of Research: Roles of the human gut microbiota and its metabolites in metabolic, neurodegenerative, cardiovascular and gastrointestinal diseases

Article Title: Roles of human gut microbiota in metabolic, neurodegenerative, cardiovascular and gastrointestinal diseases

Article References: Joshi, D., Chauhan, K., Oberoi, H. S., Kumar, D., & Taneja, N. K. (2026). Roles of human gut microbiota in metabolic, neurodegenerative, cardiovascular and gastrointestinal diseases. Discover Biotechnology, 3(1), Article 8. https://doi.org/10.1007/s44340-026-00053-2

Image Credits: AI Generated

DOI: 10.1007/s44340-026-00053-2

Keywords: gut microbiota, dysbiosis, short-chain fatty acids, TMAO, gut-brain axis, Parkinson's disease, Alzheimer's disease, hypertension, atherosclerosis, obesity, diabetes, fecal microbiota transplantation

This revelation is transformative, as it suggests the bacterial populations within a single species may differ profoundly in how they function and interact with the host, and consequently, how they influence health and disease. Traditional classification methods tend to obscure these critical distinctions, lumping together populations that are evolutionarily and functionally divergent. This lack of granularity has often hindered efforts to pinpoint which bacteria contribute to health or pathology and which are neutral or even protective. By transcending the species-level taxonomy, the new research establishes a biological framework that more precisely reflects bacterial adaptation and niche specialization, promising a paradigm shift in microbiome science.

The study harnessed an extensive dataset, including thousands of isolated gut bacterial genomes alongside vast metagenomic sequences obtained from diverse global populations spanning various ages and health statuses. Metagenomics, the sequencing of all genetic material in a microbial community, allows scientists to capture a comprehensive snapshot of the gut’s microbial inhabitants without depending solely on cultivation methods. The researchers applied a novel computational method rooted in the principles of reverse ecology—a technique that infers ecological and evolutionary adaptations directly from genomic data—to detect genetic signatures indicative of recent natural selection and adaptation within gut bacteria.

A particularly striking feature identified by this methodology is the phenomenon of genome-wide selective sweeps. These occur when a beneficial mutation arises in an individual bacterium and rapidly proliferates through the population, effectively displacing genetic variants and reducing diversity across the genome. This process generates highly homogeneous but distinct bacterial populations that can be readily distinguished in genomic analyses. The team discovered that what were traditionally categorized as single bacterial species actually consist of multiple such lineages, each defined by its unique evolutionary trajectory and ecological specialization within the gut milieu.

These evolutionarily distinct bacterial populations are not randomly distributed but show clear associations with specific human conditions. For example, some populations correlate strongly with advanced age, while others have been linked to chronic inflammatory bowel diseases, colorectal cancer, and type 2 diabetes. This finding underscores the profound interaction between microbial evolution and human health, suggesting that the microbiome’s impact on disease may depend on the presence or absence of particular bacterial lineages rather than broad species categories.

Moreover, the research reveals a dynamic global landscape of gut microbiota evolution and dispersal. Contrary to previous assumptions that strains remain relatively localized, evidence points to certain bacterial populations rapidly spreading worldwide within mere decades. This observation previously was well-documented in pathogenic bacteria but had not been appreciated to the same extent among commensal gut species. Such rapid global dissemination suggests that ecological units within the microbiome are capable of adapting to new environments and hosts with remarkable agility.

These findings carry profound implications for our understanding of microbial ecology and biogeography. They challenge the conventional wisdom that lifestyle factors alone—diet, medication, or hygiene—shape the human gut microbiome. Instead, the transmission of specific bacterial populations between individuals and communities emerges as a critical driver of microbiome composition and evolution, emphasizing the microbiome’s social and environmental interconnectedness across populations.

From a clinical perspective, these insights open exciting avenues for more precise diagnostics and therapeutic interventions. Current microbiome-based medical strategies often fall short because they target entire species without recognizing the heterogeneity of functional adaptations among bacterial subpopulations. By distinguishing the biologically relevant evolutionary units, it becomes feasible to identify specific lineages that contribute to disease or promote health. This precision offers the potential to develop tailored microbiome therapies, such as selectively augmenting beneficial strains or suppressing harmful ones, thereby enhancing treatment efficacy and minimizing unintended consequences.

Looking forward, the University of Vienna team plans to delve deeper into the genetic underpinnings that differentiate these bacterial populations. By elucidating which genes are subject to selection and how they confer ecological advantages, researchers aim to uncover the molecular mechanisms driving adaptation and functionality in the human gut. Such knowledge could lead to targeted manipulation of microbial functions, further refining microbiome-based therapies and personalized medicine approaches.

The methodological advances exemplified by this work represent a significant leap in microbiome science, blending evolutionary biology, ecology, and genomics in a holistic framework. This interdisciplinary synergy enables a more accurate picture of microbial diversity and its relationship with the host, overcoming the limitations of traditional taxonomic systems and unlocking new layers of insight into the microbiome’s complexity.

In sum, the University of Vienna’s research shines a spotlight on the dynamic evolutionary landscape within our own gastrointestinal tract. It reveals a mosaic of specialized bacterial populations shaped by natural selection and ecological opportunity, many of which have direct implications for human health. This newfound understanding elevates our ability to diagnose, monitor, and modulate the microbiome with unprecedented precision, ushering in a new era of microbiome research and medicine that celebrates the intricate evolutionary ecology of our microbial companions.

As the scientific community continues to unravel the human microbiome’s mysteries, the integration of evolutionary adaptation into microbial classification promises to refine how we interpret the roles of gut bacteria in health and disease. Far beyond cataloging microbial species, this approach shines a light on the ecological units that truly matter, offering hope for transformative advances in healthcare informed by the subtle but powerful forces of evolution within the human body.

Subject of Research: Human gut microbiome, bacterial population genetics, microbiome adaptation and ecology, disease association.

Article Title: Genome-wide sweeps create ecological units in the human gut microbiome.

News Publication Date: 6-May-2026.

Web References:
https://doi.org/10.1038/s41586-026-10476-w

References: Published in Nature, DOI: 10.1038/s41586-026-10476-w.

Keywords: human gut microbiome, reverse ecology, genome-wide selective sweeps, bacterial evolution, microbial adaptation, metagenomics, microbial populations, disease association, microbiome therapy, ecological niches, bacterial lineage dispersal, microbiome diagnostics.

Hepatic steatosis, characterized by excessive fat accumulation in liver cells, has become a global health concern due to its association with obesity, type 2 diabetes, and cardiovascular disease. Traditionally, the condition has been linked to high caloric intake, sedentary lifestyles, and excessive consumption of fructose-rich foods such as sugary beverages and processed snacks. However, pinpointing the causative mechanisms and developing effective interventions have remained significant challenges. This new research points to the gut microbiome — the diverse community of microorganisms inhabiting the human intestine — as a central player that can modulate the liver’s response to dietary fructose.

The study elucidates the molecular and microbial mechanisms by which dietary fibers influence the gut ecosystem. Dietary fiber, an indigestible carbohydrate, undergoes fermentation by specific gut bacteria, producing bioactive metabolites. These metabolites appear to enhance the metabolic capacity of the host, particularly in processing fructose, thereby preventing its accumulation and subsequent conversion into liver fat. The authors employed state-of-the-art metagenomic sequencing and metabolomic profiling to reveal how fiber supplementation promotes the growth of distinct bacterial populations capable of transforming fructose into less harmful compounds.

One of the remarkable findings from the research is the identification of a “fiber-adapted” microbiome phenotype, which differs markedly from microbiomes shaped by low-fiber diets. Mice that received a high-fiber diet exhibited an expanded population of commensal bacteria, including members of the Bacteroides and Akkermansia genera, which correlated with enhanced fructose metabolism and reduced liver fat deposition. This adaptation was reversible, suggesting that dietary interventions can dynamically remodel the gut ecosystem to foster metabolic health.

To delve into the causal relationship, the scientists conducted fecal microbiota transplants (FMT) between mice fed either a high-fiber or low-fiber diet. Remarkably, transplanting the fiber-adapted microbiome into mice consuming a fructose-rich diet reduced hepatic steatosis even without altering the recipient animals’ diet. This finding not only implicates the gut microbiome as a mediator of fructose metabolism but also opens avenues for microbiome-targeted therapies against fatty liver disease.

Furthermore, the study provides insights into the enzymatic pathways engaged by the fiber-adapted microbiota in fructose clearance. Specific bacterial enzymes, including fructokinases and aldolases, were upregulated, enhancing microbial fructose utilization. By channeling fructose metabolism away from the host’s liver and into microbial fermentation pathways, these bacteria help alleviate metabolic stress and lipid accumulation in hepatocytes. This shift represents a novel paradigm in host-microbe metabolic cooperation.

The implications of this discovery extend into potential nutritional guidelines and clinical practices. Given the global increase in fructose consumption and the rising prevalence of non-alcoholic fatty liver disease (NAFLD), dietary fiber supplementation could be leveraged as a non-pharmacological strategy to modulate gut microbiota and protect liver health. Unlike interventions targeting host metabolism directly, manipulating the microbiome represents a systemic approach that can complement existing treatments for metabolic syndrome and its sequelae.

Another compelling aspect of the study is its demonstration of the reversibility of hepatic steatosis through gut microbiome modulation, independent of weight loss. This decoupling challenges the conventional wisdom that weight reduction is a prerequisite for improvements in liver pathology, underscoring the microbiome’s direct influence. Thus, individuals unable to achieve or maintain weight loss might still benefit metabolically from dietary fiber-induced microbiome shifts.

The researchers also shed light on the cross-talk between gut-derived metabolites and host signaling pathways involved in lipid metabolism. Short-chain fatty acids (SCFAs), produced through bacterial fermentation of dietary fiber, were elevated in fiber-fed mice and shown to enhance insulin sensitivity and reduce inflammatory markers in the liver. These bioactive molecules serve as metabolic intermediaries, bridging microbial activity and host physiology, thereby reinforcing the significance of the gut-liver axis.

This investigation also paves the way for future precision nutrition approaches. Given the heterogeneity in human gut microbiomes, personalized dietary fiber regimens tailored to individual microbial profiles could optimize fructose clearance and hepatic health. Ongoing research aims to identify biomarkers predictive of microbiome responsiveness to fiber interventions, potentially enabling clinicians to customize therapeutic strategies in real time.

From a broader scientific perspective, the study exemplifies the transformative power of integrating multi-omics technologies—metagenomics, metabolomics, transcriptomics—to unravel complex biological systems. This systems-level approach not only provides mechanistic depth but also identifies actionable targets for intervention. As such, the field moves closer to translating microbiome science into clinical realities for metabolic disorders.

In addition to metabolic health, the findings may have implications for other diseases linked to altered gut microbiota and fructose metabolism, such as cardiovascular disease and certain cancers. By harnessing the gut microbiome’s metabolic plasticity through diet, a new frontier emerges for preventive medicine and sustainable health interventions.

This research also sparks intriguing questions regarding the evolutionary basis of host-microbiome interactions and dietary adaptations. The ability of the gut microbiome to adapt rapidly to dietary changes and influence host metabolism underscores its role as a dynamic organ, potentially shaped by millennia of co-evolution with human dietary patterns.

In conclusion, the revelation that a dietary fiber-adapted gut microbiome can clear dietary fructose and reverse hepatic steatosis marks a watershed moment in metabolic research. This discovery signals a paradigm shift, emphasizing the gut microbiome not merely as a passive resident but as an active participant in metabolic homeostasis. As the scientific community continues to uncover the complexities of this relationship, the prospect of harnessing diet-microbiome synergy to combat metabolic diseases remains an exciting and promising horizon.

Subject of Research: Dietary fiber-induced gut microbiome adaptation and its role in fructose metabolism and hepatic steatosis reversal

Article Title: Dietary fibre-adapted gut microbiome clears dietary fructose and reverses hepatic steatosis

Article References:
Jung, S., Bae, H., Song, WS. et al. Dietary fibre-adapted gut microbiome clears dietary fructose and reverses hepatic steatosis. Nat Metab (2025). https://doi.org/10.1038/s42255-025-01356-0

Image Credits: AI Generated

The body’s microbiome is a complex ecosystem, teeming with trillions of microorganisms that play essential roles in maintaining health. However, this delicate balance can be disrupted, leading to dysbiosis, which has been linked to numerous health issues beyond the gut itself, including obesity, diabetes, and cardiovascular diseases. The new findings by Zhang and colleagues suggest that the gut microbiota not only has a role in the regulation of metabolic processes but is also crucial in how the body responds to heart failure.

Heart failure is a leading cause of morbidity and mortality worldwide, characterized by the heart’s inability to pump sufficiently to maintain blood flow to meet the body’s needs. Traditional treatment strategies focus primarily on the cardiovascular system, often overlooking the critical interplay between the heart and the microbiome. By illuminating the mechanistic insights into this relationship, Zhang et al. provide a vital piece of the puzzle that could lead to innovative therapies.

The LPS-TLR4 signaling pathway is a key player in the immune response, and dysregulation here can trigger a cascade of inflammatory activities that worsen heart failure. LPS, a component of bacterial cell walls, can induce strong immune responses. When TLR4, a receptor on immune cells, recognizes LPS, it triggers the NF-κB signaling pathway, leading to the expression of pro-inflammatory cytokines and contributing to cardiac inflammation and dysfunction. Understanding this pathway enables researchers to see how an imbalance in gut bacteria can lead to the toll on heart health.

Zhang’s research corroborates previous studies suggesting that microbial metabolites can influence cardiomyocyte function and overall heart performance. Among these metabolites, short-chain fatty acids (SCFAs) produced by the fermentation of dietary fibers in the gut have garnered interest for their protective effects against heart failure. They can modulate inflammation, promote insulin sensitivity, and improve endothelial function. The researchers propose that correcting dysbiosis may lead to improved generation of these beneficial metabolites, ultimately benefiting heart function.

Moreover, the results of the study indicate potential therapeutic strategies targeting TLR4 inhibition as a means of countering the adverse effects of gut microbiota dysbiosis on heart health. With the use of TLR4 antagonists or inhibitors, it may be possible to mitigate the inflammatory responses that exacerbate heart failure. This represents a promising avenue for treatment, as current therapies primarily focus on managing symptoms rather than addressing the underlying causes.

Additionally, the researchers emphasize the importance of diet in shaping the microbiome and, consequently, heart health. A balanced diet rich in fiber, probiotics, and prebiotics can foster a healthy gut microbiota, potentially reducing the risk of heart failure. Interventions aimed at dietary changes could be a simple yet effective complement to pharmacological treatments, providing an added layer of protection against heart failure.

The findings from Zhang et al. contribute to a growing body of literature that seeks to interconnect microbiology with cardiology, reshaping how we view chronic diseases and their treatments. By highlighting the gut-heart axis, this research opens up new possibilities for multidimensional therapeutic approaches that are more holistic and comprehensive.

As the study calls for further exploration, the implications extend beyond heart failure alone. Understanding how gut microbiota communicates with the immune system and other body processes could yield insights into a range of cardiovascular diseases and conditions. Future research may focus on developing personalized approaches, where microbiome assessments guide therapeutic decisions tailored to individual patients.

Overall, this study serves as a compelling reminder of the complexity of human health and the interplay of various systems within the body. Emphasizing the gut microbiota’s role in impacting cardiovascular health and the underlying signaling pathways involved can lead to groundbreaking new therapies that reach beyond the confines of traditional medicine.

In conclusion, the work of Zhang and colleagues offers a profound perspective on how we approach heart failure treatment. It emphasizes the need for a holistic understanding of health that goes beyond mere symptom management and seeks to rectify underlying imbalances contributing to disease. The journey towards refining our therapeutic landscape may well lie in this innovative intersection of microbiome research and cardiovascular care.

Subject of Research: The connection between gut microbiota dysbiosis and heart failure exacerbation.

Article Title: Correction: Gut microbiota dysbiosis exacerbates heart failure by the LPS-TLR4/NF-κB signalling axis: mechanistic insights and therapeutic potential of TLR4 inhibition.

Article References:

Zhang, C., Teng, X., Cao, Q. et al. Correction: Gut microbiota dysbiosis exacerbates heart failure by the LPS-TLR4/NF-κB signalling axis: mechanistic insights and therapeutic potential of TLR4 inhibition. J Transl Med 23, 954 (2025). https://doi.org/10.1186/s12967-025-06943-z

Image Credits: AI Generated

DOI:

Keywords: Gut microbiota, heart failure, dysbiosis, inflammation, TLR4, NF-κB, SCFAs, microbiome, therapeutic potential, cardiovascular health.