肠道菌群DNA修复机制:2024氧化应激与药物调控新进展

18小时前 MedSci xAi 发表于广东省
本文解析肠道微生物DNA修复机制激活原理,详述氧化应激、抗生素压力等遗传损伤因素如何影响菌群功能平衡,并探讨药物靶向调控COG功能基因恢复代谢稳态的分子机制。
Elevated DNA repair abundance typically indicates that the microbial community is experiencing genetic damage stress (such as oxidative stress or antibiotics), thereby activating repair mechanisms. The activation of antioxidant responses directly reflects an abnormal state of oxidative stress in the gut microenvironment. Changes in amino acid transport can directly impact the production of microbial metabolites (such as short-chain fatty acids, SCFAs) and host nutrient supply. Overexpression of antimicrobial peptide synthesis may disrupt the competitive balance among microbial communities, becoming an intrinsic driving factor for dysbiosis (34). However, the regulatory effects of drugs can restore these functions to normal levels, maintaining the functional balance of the gut microbiota. The reduced abundance of functional genes related to substance transport and metabolic regulation, such as COG1379, COG3741, COG0398, COG1639, and COG5607, further confirms the targeted nature of drug effects on gut microbial metabolic functions, preventing metabolic dysfunction in the gut and providing a stable metabolic environment for mucosal repair and immune regulation.
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