Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation
Cell Regeneration, ISSN: 2045-9769, Vol: 13, Issue: 1, Page: 2
2024
- 1Citations
- 5Captures
- 1Mentions
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- Citations1
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Research Data from Imperial College London Update Understanding of Health and Medicine (Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation)
2024 MAR 19 (NewsRx) -- By a News Reporter-Staff News Editor at NewsRx Cardiovascular Daily -- Investigators publish new report on agriculture. According to news
Article Description
The regenerative capacity of the adult mammalian heart remains a formidable challenge in biological research. Despite extensive investigations into the loss of regenerative potential during evolution and development, unlocking the mechanisms governing cardiomyocyte proliferation remains elusive. Two recent groundbreaking studies have provided fresh perspectives on mitochondrial-to-nuclear communication, shedding light on novel factors that regulate cardiomyocyte proliferation. The studies identified two mitochondrial processes, fatty acid oxidation and protein translation, as key players in restricting cardiomyocyte proliferation. Inhibition of these processes led to increased cell cycle activity in cardiomyocytes, mediated by reduction in H3k4me3 levels through accumulated α-ketoglutarate (αKG), and activation of the mitochondrial unfolded protein response (UPR), respectively. In this research highlight, we discuss the novel insights into mitochondrial-to-nuclear communication presented in these studies, the broad implications in cardiomyocyte biology and cardiovascular diseases, as well as the intriguing scientific questions inspired by the studies that may facilitate future investigations into the detailed molecular mechanisms of cardiomyocyte metabolism, proliferation, and mitochondrial-to-nuclear communications.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85183626075&origin=inward; http://dx.doi.org/10.1186/s13619-024-00186-x; http://www.ncbi.nlm.nih.gov/pubmed/38291287; https://cellregeneration.springeropen.com/articles/10.1186/s13619-024-00186-x; https://dx.doi.org/10.1186/s13619-024-00186-x
Springer Science and Business Media LLC
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