{"title":"线粒体功能障碍加速衰老。","authors":"Johannes Schroth, Sian M Henson","doi":"10.20900/immunometab20200035","DOIUrl":null,"url":null,"abstract":"<p><p>We review here the seminal findings of Desdin-Mico et al. showing that T cells with dysfunctional mitochondria induce multimorbity and premature senescence, due to mitochondrial transcription factor A (TFAM). They add further weight to the idea that targeting immunometabolism could be beneficial in combating the detrimental effects of age-related disease.</p>","PeriodicalId":13361,"journal":{"name":"Immunometabolism","volume":"2 4","pages":"e200035"},"PeriodicalIF":0.0000,"publicationDate":"2020-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7116259/pdf/","citationCount":"3","resultStr":"{\"title\":\"Mitochondrial Dysfunction Accelerates Ageing.\",\"authors\":\"Johannes Schroth, Sian M Henson\",\"doi\":\"10.20900/immunometab20200035\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>We review here the seminal findings of Desdin-Mico et al. showing that T cells with dysfunctional mitochondria induce multimorbity and premature senescence, due to mitochondrial transcription factor A (TFAM). They add further weight to the idea that targeting immunometabolism could be beneficial in combating the detrimental effects of age-related disease.</p>\",\"PeriodicalId\":13361,\"journal\":{\"name\":\"Immunometabolism\",\"volume\":\"2 4\",\"pages\":\"e200035\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-10-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7116259/pdf/\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Immunometabolism\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.20900/immunometab20200035\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Immunometabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.20900/immunometab20200035","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
We review here the seminal findings of Desdin-Mico et al. showing that T cells with dysfunctional mitochondria induce multimorbity and premature senescence, due to mitochondrial transcription factor A (TFAM). They add further weight to the idea that targeting immunometabolism could be beneficial in combating the detrimental effects of age-related disease.
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