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Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury
Acute Kidney Injury (AKI), a critical clinical syndrome, has been strongly linked to mitochondrial malfunction. Mitochondria, vital cellular organelles, play a key role in regulating cellular energy metabolism and ensuring cell survival. Impaired mitochondrial function in AKI leads to decreased ener...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10456901/ https://www.ncbi.nlm.nih.gov/pubmed/37635869 http://dx.doi.org/10.3389/fcell.2023.1244313 |
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author | Hao, Yajie Zhao, Limei Zhao, Jing Yu Han, Xiutao Zhou, Xiaoshuang |
author_facet | Hao, Yajie Zhao, Limei Zhao, Jing Yu Han, Xiutao Zhou, Xiaoshuang |
author_sort | Hao, Yajie |
collection | PubMed |
description | Acute Kidney Injury (AKI), a critical clinical syndrome, has been strongly linked to mitochondrial malfunction. Mitochondria, vital cellular organelles, play a key role in regulating cellular energy metabolism and ensuring cell survival. Impaired mitochondrial function in AKI leads to decreased energy generation, elevated oxidative stress, and the initiation of inflammatory cascades, resulting in renal tissue damage and functional impairment. Therefore, mitochondria have gained significant research attention as a potential therapeutic target for AKI. Mitochondrial dynamics, which encompass the adaptive shifts of mitochondria within cellular environments, exert significant influence on mitochondrial function. Modulating these dynamics, such as promoting mitochondrial fusion and inhibiting mitochondrial division, offers opportunities to mitigate renal injury in AKI. Consequently, elucidating the mechanisms underlying mitochondrial dynamics has gained considerable importance, providing valuable insights into mitochondrial regulation and facilitating the development of innovative therapeutic approaches for AKI. This comprehensive review aims to highlight the latest advancements in mitochondrial dynamics research, provide an exhaustive analysis of existing studies investigating the relationship between mitochondrial dynamics and acute injury, and shed light on their implications for AKI. The ultimate goal is to advance the development of more effective therapeutic interventions for managing AKI. |
format | Online Article Text |
id | pubmed-10456901 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-104569012023-08-26 Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury Hao, Yajie Zhao, Limei Zhao, Jing Yu Han, Xiutao Zhou, Xiaoshuang Front Cell Dev Biol Cell and Developmental Biology Acute Kidney Injury (AKI), a critical clinical syndrome, has been strongly linked to mitochondrial malfunction. Mitochondria, vital cellular organelles, play a key role in regulating cellular energy metabolism and ensuring cell survival. Impaired mitochondrial function in AKI leads to decreased energy generation, elevated oxidative stress, and the initiation of inflammatory cascades, resulting in renal tissue damage and functional impairment. Therefore, mitochondria have gained significant research attention as a potential therapeutic target for AKI. Mitochondrial dynamics, which encompass the adaptive shifts of mitochondria within cellular environments, exert significant influence on mitochondrial function. Modulating these dynamics, such as promoting mitochondrial fusion and inhibiting mitochondrial division, offers opportunities to mitigate renal injury in AKI. Consequently, elucidating the mechanisms underlying mitochondrial dynamics has gained considerable importance, providing valuable insights into mitochondrial regulation and facilitating the development of innovative therapeutic approaches for AKI. This comprehensive review aims to highlight the latest advancements in mitochondrial dynamics research, provide an exhaustive analysis of existing studies investigating the relationship between mitochondrial dynamics and acute injury, and shed light on their implications for AKI. The ultimate goal is to advance the development of more effective therapeutic interventions for managing AKI. Frontiers Media S.A. 2023-08-11 /pmc/articles/PMC10456901/ /pubmed/37635869 http://dx.doi.org/10.3389/fcell.2023.1244313 Text en Copyright © 2023 Hao, Zhao, Zhao, Han and Zhou. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cell and Developmental Biology Hao, Yajie Zhao, Limei Zhao, Jing Yu Han, Xiutao Zhou, Xiaoshuang Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title | Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title_full | Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title_fullStr | Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title_full_unstemmed | Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title_short | Unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
title_sort | unveiling the potential of mitochondrial dynamics as a therapeutic strategy for acute kidney injury |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10456901/ https://www.ncbi.nlm.nih.gov/pubmed/37635869 http://dx.doi.org/10.3389/fcell.2023.1244313 |
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