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We found that human mesenchymal stem cells (hMSCs) were sensitive to MAVS deficiency, as manifested by accelerated senescence phenotypes. We uncovered that the role of MAVS in maintaining mitochondrial structural integrity and functional homeostasis depends on its interaction with the guanosine triphosphatase optic atrophy type 1 (OPA1). Depletion of MAVS or OPA1 led to the dysfunction of mitochondria and cellular senescence, whereas replenishment of MAVS or OPA1 in MAVS-knockout hMSCs alleviated mitochondrial defects and premature senescence phenotypes. Taken together, our data underscore an uncanonical role of MAVS in safeguarding mitochondrial homeostasis and antagonizing human stem cell senescence.<\/jats:p>","DOI":"10.34133\/research.0192","type":"journal-article","created":{"date-parts":[[2023,6,23]],"date-time":"2023-06-23T06:18:18Z","timestamp":1687501098000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark_01","source":"Crossref","is-referenced-by-count":27,"title":["MAVS Antagonizes Human Stem Cell Senescence as a Mitochondrial Stabilizer"],"prefix":"10.34133","volume":"6","author":[{"given":"Cui","family":"Wang","sequence":"first","affiliation":[{"name":"CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, \rChinese Academy of Sciences and China National Center for Bioinformation, Beijing 100101, China."},{"name":"University of Chinese Academy of Sciences, Beijing 100049, 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