Table 1_Angiotensin converting enzyme inhibitors and angiotensin receptor blockers impact on the gut microbiome: a systematic review.docx

BackgroundInhibition of the renin–angiotensin system (RAS) may influence gut microbial composition and blood pressure, yet current evidence remains limited. This review examines how angiotensin-converting enzyme inhibitors (ACEis) and angiotensin receptor blockers (ARBs) modify gut microbiome composition, function, and blood pressure regulation.
MethodsWe conducted a systematic search of MEDLINE and EMBASE from inception to September 2025 using terms including “human,” “rat,” “angiotensin converting enzyme inhibitor,” “angiotensin receptor blocker,” and “gut microbiome.” Eligible studies were required to report changes in microbiome diversity, bacterial composition, or short-chain fatty acids (SCFAs) associated with ACEi/ARB treatment across animal or human models. Data extraction and risk of bias assessments were performed independently by multiple reviewers.
ResultsAfter deduplication, 642 retrieved articles were filtered and nine met inclusion criteria (eight in rodent models, one human study). ACEi/ARB administration in animals was associated with increased microbial diversity, restoration of intestinal oxygen balance, and enrichment of SCFA-producing anaerobic genera such as Bifidobacterium, Bacteroides, Blautia, and Akkermansia. In the human study, ACEi/ARB use did not significantly alter microbial diversity, but decreased populations of facultative aerobic pathogens including Staphylococcus and Enterobacterales. Functionally, prolonged RAS inhibition elevated levels of acetate, propionate, and butyrate, and enhanced gut barrier integrity while attenuating inflammatory signaling. The human study was found to have a moderate risk of bias.
ConclusionsACEi and ARB therapies appear to reshape gut microbiome structure and metabolic function, promoting SCFA-producer expansion, improved gut barrier integrity, and modulation of microbial taxa linked to inflammation and hypertension. However, human data is limited, and further transitional research is needed to confirm these findings.

背景 肾素-血管紧张素系统（renin–angiotensin system, RAS）的抑制作用或可影响肠道微生物组（gut microbiome）组成与血压水平，但目前相关证据仍较为有限。本综述旨在探讨血管紧张素转换酶抑制剂（angiotensin-converting enzyme inhibitors, ACEis）与血管紧张素受体拮抗剂（angiotensin receptor blockers, ARBs）如何调控肠道微生物组的组成、功能及血压调节过程。
方法 本研究以建库至2025年9月的MEDLINE和EMBASE数据库为检索源，采用“human”“rat”“angiotensin converting enzyme inhibitor”“angiotensin receptor blocker”“gut microbiome”等关键词开展系统检索。纳入标准要求研究需报告动物或人体模型中，接受ACEi/ARB治疗后微生物组多样性、细菌组成或短链脂肪酸（short-chain fatty acids, SCFAs）的变化情况。数据提取与偏倚风险评估由多名研究者独立完成。
结果 去重后，共筛选出642篇检索得到的文献，其中9篇符合纳入标准（8项为啮齿动物模型研究，1项为人体研究）。动物实验中，ACEi/ARB给药与微生物组多样性升高、肠道氧平衡恢复以及产SCFA的厌氧菌属（如双歧杆菌属Bifidobacterium、拟杆菌属Bacteroides、布劳特氏菌属Blautia以及嗜黏蛋白阿克曼菌属Akkermansia）的富集显著相关。在人体研究中，ACEi/ARB的使用未显著改变微生物组多样性，但降低了包括葡萄球菌属Staphylococcus和肠杆菌目Enterobacterales在内的兼性需氧病原菌的丰度。从功能层面来看，长期RAS抑制可升高乙酸、丙酸与丁酸的水平，增强肠道屏障完整性并减轻炎症信号通路活化。该人体研究存在中度偏倚风险。
结论 ACEi与ARB治疗似乎可重塑肠道微生物组结构与代谢功能，促进产SCFA菌属的扩增，改善肠道屏障完整性，并调节与炎症及高血压相关的微生物类群。但目前相关人体数据较为有限，需开展进一步转化研究以验证上述发现。