文献类型：期刊文献

英文题名：The microbiome-mitochondria axis: the context-dependent role of urolithin A in aging and cancer via mitophagy

作者：Wu, Jiayuan[1];Ye, Xinxin[1];Hua, Wei[1];Yao, Yuyang[5];Sun, Lu[1];Ma, Hongyu[1];Yu, Congcong[1];Cheng, Yanling[1,3,4];Mi, Shengquan[1,2]

第一作者：Wu, Jiayuan

通讯作者：Mi, SQ[1];Mi, SQ[2]

机构：[1]Beijing Union Univ, Coll Biochem Engn, 18 Fatou Xili 3 Qu, Beijing, Peoples R China;[2]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing, Peoples R China;[3]Univ Minnesota, Ctr Biorefining, St Paul, MN USA;[4]Univ Minnesota, Dept Bioprod & Biosyst Engn, St Paul, MN USA;[5]Beijing Technol & Business Univ, Beijing 100048, Peoples R China

第一机构：北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Coll Biochem Engn, 18 Fatou Xili 3 Qu, Beijing, Peoples R China;[2]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing, Peoples R China.|[114172]北京联合大学应用文理学院;[11417]北京联合大学;[1141726]北京联合大学生物化学工程学院;

年份：2026

卷号：53

期号：1

外文期刊名：MOLECULAR BIOLOGY REPORTS

收录：;Scopus(收录号：2-s2.0-105046472372);WOS:【SCI-EXPANDED(收录号:WOS:001841189500009)】；

语种：英文

外文关键词：Urolithin A; Mitophagy; Gut microbiota; Urolithin metabotype; Aging; Cancer

摘要：Urolithin A (UA) is a gut microbiota-derived metabolite formed from dietary ellagitannins and ellagic acid. It has drawn sustained interest because it can influence mitochondrial quality control, but the evidence does not support a simple anti-aging or anticancer label. In this review, UA is examined across microbial metabolism, urolithin metabotypes, pharmacokinetic exposure, mitophagy biology, aging-related phenotypes, and cancer. The emphasis is placed on what has been shown, what remains model-dependent, and where translational claims are still premature. Preclinical work links UA to PINK1/Parkin-, TFEB-, AMPK-, sirtuin-, and Nrf2-associated pathways, with reported improvements in mitochondrial turnover and inflammatory signaling. Human data are narrower: most trials have been short and have focused on safety, muscle performance, mitochondrial signatures, and circulating biomarkers. Evidence for cancer prevention or cancer therapy still comes mainly from cell and animal studies. Because mitophagy can limit early mitochondrial damage but may also help established tumors survive hypoxia, nutrient restriction, dormancy, and therapy-induced stress, UA is better regarded as a microbiome-dependent mitochondrial modulator whose effects depend on biological setting. The next step is to define direct molecular targets, test native and conjugated UA at human-relevant exposure ranges, account for UM-A, UM-B, and UM-0 metabotypes, and evaluate cancer-specific endpoints before making therapeutic claims.