Primary sarcopenia (PS) is an age-related degenerative disorder characterized by progressive loss of skeletal muscle mass and function. This review delineates three mechanisms whereby gut dysbiosis drives PS pathogenesis: decreased secondary bile acids inhibit farnesoid X receptor signaling, thereby attenuating muscle protein synthesis; disrupted short-chain fatty acid metabolism weakens free fatty acid receptor 2/adenosine monophosphate-activated protein kinase signaling, aggravating proteolysis and mitochondrial dysfunction; gut barrier impairment activates the endotoxin–Toll-like receptor 4-mediated inflammatory cascade, accelerating ubiquitin-proteasome system activation. Interventional evidence confirms that microbiota-targeted therapies (probiotics regulating bile acid metabolism and prebiotics enhancing short-chain fatty acid production) effectively improve muscle function. By synthesizing molecular evidence of the “gut-muscle axis”, this review offers theoretical references for developing PS prevention and treatment strategies.
[Abstract]The pathogenesis of aortic disease is not fully understood. Gut dysbiosis may play a role in the occurrence and development of aortic diseases. Several studies showed that the diversity of microbiota in abdominal aortic aneurysms significantly decreases and is correlated with the diameter of the aneurysm. Characteristic microbial communities associated with abdominal aortic aneurysm, such as Roseburia, Bifidobacterium, Ruminococcus, Akkermansia have been found in human and animal studies. The gut microbiota of patients with aortic dissection varies greatly. Characteristic microbial communities like Lachnospiraceae and Ruminococcus present a potential impact on the pathogenesis of aortic dissection. Bifidobacterium may be associated with Takayasu arteritis and thoracic aortic aneurysm. The gut microbiota affects the physiological functions of the host by synthesizing bioactive metabolites, which causes aortic diseases, mainly involving metabolites such as trimethylamine N-oxide (TMAO), lipopolysaccharides (LPS), tryptophan, and short chain fatty acids. More and more evidence supports the causal relationship between gut microbiota dysbiosis and aortic disease. Clarifying abnormal changes in gut microbiota may provide clues for finding potential therapeutic targets.