线粒体与细胞核之间的通讯通过多种途径调节心肌细胞的增殖。

IF 4 Q2 CELL & TISSUE ENGINEERING Cell Regeneration Pub Date : 2024-01-31 DOI:10.1186/s13619-024-00186-x
Xinhang Li, Yalin Zhu, Pilar Ruiz-Lozano, Ke Wei
{"title":"线粒体与细胞核之间的通讯通过多种途径调节心肌细胞的增殖。","authors":"Xinhang Li, Yalin Zhu, Pilar Ruiz-Lozano, Ke Wei","doi":"10.1186/s13619-024-00186-x","DOIUrl":null,"url":null,"abstract":"<p><p>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<sup>mt</sup>), 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.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"13 1","pages":"2"},"PeriodicalIF":4.0000,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10828256/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation.\",\"authors\":\"Xinhang Li, Yalin Zhu, Pilar Ruiz-Lozano, Ke Wei\",\"doi\":\"10.1186/s13619-024-00186-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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<sup>mt</sup>), 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.</p>\",\"PeriodicalId\":9811,\"journal\":{\"name\":\"Cell Regeneration\",\"volume\":\"13 1\",\"pages\":\"2\"},\"PeriodicalIF\":4.0000,\"publicationDate\":\"2024-01-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10828256/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Regeneration\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/s13619-024-00186-x\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CELL & TISSUE ENGINEERING\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Regeneration","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/s13619-024-00186-x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL & TISSUE ENGINEERING","Score":null,"Total":0}
引用次数: 0

摘要

成年哺乳动物心脏的再生能力仍然是生物学研究中的一项艰巨挑战。尽管对进化和发育过程中再生潜能的丧失进行了广泛的研究,但对心肌细胞增殖机制的揭示仍然遥遥无期。最近的两项突破性研究为线粒体与核之间的通讯提供了新的视角,揭示了调节心肌细胞增殖的新因素。研究发现,脂肪酸氧化和蛋白质翻译这两个线粒体过程是限制心肌细胞增殖的关键因素。抑制这两个过程会导致心肌细胞的细胞周期活动增加,分别通过累积的α-酮戊二酸(αKG)降低H3k4me3水平和激活线粒体未折叠蛋白反应(UPRmt)来介导。在本研究集锦中,我们将讨论这些研究对线粒体-核通讯的新见解、对心肌细胞生物学和心血管疾病的广泛影响,以及由这些研究启发的引人入胜的科学问题,这些问题可能会促进未来对心肌细胞代谢、增殖和线粒体-核通讯的详细分子机制的研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Mitochondrial-to-nuclear communications through multiple routes regulate cardiomyocyte proliferation.

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 (UPRmt), 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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Cell Regeneration
Cell Regeneration Biochemistry, Genetics and Molecular Biology-Cell Biology
CiteScore
5.80
自引率
0.00%
发文量
42
审稿时长
35 days
期刊介绍: Cell Regeneration aims to provide a worldwide platform for researches on stem cells and regenerative biology to develop basic science and to foster its clinical translation in medicine. Cell Regeneration welcomes reports on novel discoveries, theories, methods, technologies, and products in the field of stem cells and regenerative research, the journal is interested, but not limited to the following topics: ◎ Embryonic stem cells ◎ Induced pluripotent stem cells ◎ Tissue-specific stem cells ◎ Tissue or organ regeneration ◎ Methodology ◎ Biomaterials and regeneration ◎ Clinical translation or application in medicine
期刊最新文献
Identification of feature genes in intestinal epithelial cell types. Application and new findings of scRNA-seq and ST-seq in prostate cancer. Beyond resorption: osteoclasts as drivers of bone formation. Subtype-specific neurons from patient iPSCs display distinct neuropathological features of Alzheimer's disease. Targeting senescent cells in aging and COVID-19: from cellular mechanisms to therapeutic opportunities.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1