Abstract
Recent technological advances have significantly enhanced our understanding of the role microbial communities play in the human body. The gut microbiota, one of the most diverse microbiomes, consists of over 35,000 bacterial species and 10 million genes, leading researchers to consider it as an additional organ. This whiles relatively stable within each individual highly influenced by exogenous and endogenous factors. Collectively, the gut microbiota functions as a "second genome", profoundly impacting the host’s metabolic pathways and regulating the body’s complex homeostatic balance.Research into the "microbe–host" interaction, both in health and disease, has garnered worldwide scientific. In chronic kidney disease (CKD), the gut microbiota undergoes significant changes, and growing evidences suggests that dysbiosis plays a crucial role in the progression of renal failure. Key pathological process, such as the production of gut-derived uremic toxins, decreased synthesis of short– chain fatty acids, altered intestinal pH, compromised intestinal barrier function, and heightened systemic inflammation, are all linked the intestinal microbiota. However, relationship between these changes and the pathogenesis and progression of kidney disease requires further investigation. Advances in microbiome research, including metagenomic and metatranscriptomic analyses, alongside proteomic, metabolomics, and immunomic studies, have greatly expanded our understanding of microbiomal community structure and functions. These technologies, coupled with mechanistic experiments in model systems, have deepened our knowledge of how the microbiome influences metabolism. Current research aims to explore the bidirectional relationship between the microbiota and the host, identifying potential interventions that could help restore a mutualistic relationship.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Similar Papers
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.