Stem cell mitochondria during aging

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• 作者：Jason Chua Min-Wen ; Elwin Tan Jun-Hao ; Ng Shyh-Chang ; ^{shyhng@gmail.com" class="auth_mail" title="E-mail the corresponding author} ; ^{ngsc1@gis.a-star.edu.sg" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Stem cells ; Mitochondria ; mtDNA ; Regeneration ; Degeneration ; Aging
• 刊名：Seminars in Cell & Developmental Biology
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：52
• 期：Complete
• 页码：110-118
• 全文大小：1536 K

文摘

Mitochondria are the central hubs of cellular metabolism, equipped with their own mitochondrial DNA (mtDNA) blueprints to direct part of the programming of mitochondrial oxidative metabolism and thus reactive oxygen species (ROS) levels. In stem cells, many stem cell factors governing the intricate balance between self-renewal and differentiation have been found to directly regulate mitochondrial processes to control stem cell behaviors during tissue regeneration and aging. Moreover, numerous nutrient-sensitive signaling pathways controlling organismal longevity in an evolutionarily conserved fashion also influence stem cell-mediated tissue homeostasis during aging via regulation of stem cell mitochondria. At the genomic level, it has been demonstrated that heritable mtDNA mutations and variants affect mammalian stem cell homeostasis and influence the risk for human degenerative diseases during aging. Because such a multitude of stem cell factors and signaling pathways ultimately converge on the mitochondria as the primary mechanism to modulate cellular and organismal longevity, it would be most efficacious to develop technologies to therapeutically target and direct mitochondrial repair in stem cells, as a unified strategy to combat aging-related degenerative diseases in the future.