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Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis

Mitochondria are vital organelles that supply ATP and other energy metabolites to meet the bioenergetics demands of the cell. In environments of stress or increased energy requirement, mitochondria are highly dynamic and can undergo biogenesis, fusion/fission, or autophagy. The transcription factor...

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Detalles Bibliográficos
Autores principales: Tung, Brian, Xia, Shuli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594694/
https://www.ncbi.nlm.nih.gov/pubmed/31245170
http://dx.doi.org/10.4172/2157-7633.1000436
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author Tung, Brian
Xia, Shuli
author_facet Tung, Brian
Xia, Shuli
author_sort Tung, Brian
collection PubMed
description Mitochondria are vital organelles that supply ATP and other energy metabolites to meet the bioenergetics demands of the cell. In environments of stress or increased energy requirement, mitochondria are highly dynamic and can undergo biogenesis, fusion/fission, or autophagy. The transcription factor family, Kruppel-Like Factor (KLF), is necessary to carry out normal cellular processes from proliferation to differentiation. Recently, its importance in metabolic homeostasis in various tissue types has gained much attention. A handful of evidence supports KLF4’s involvement in regulating mitochondrial homeostasis in both healthy and cancer cells. In this review, we aim to summarize the available literature that demonstrates KLF4’s ability to modulate the mitochondrial life cycle in: Cardiac tissue, in which KLF4-knockdown subsequently leads to Heart Failure (HF), and Glioblastoma (GBM), where its expression promotes extensive mitochondrial fusion and offers mild cell protection under serum-deprivation.
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spelling pubmed-65946942019-06-26 Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis Tung, Brian Xia, Shuli J Stem Cell Res Ther Article Mitochondria are vital organelles that supply ATP and other energy metabolites to meet the bioenergetics demands of the cell. In environments of stress or increased energy requirement, mitochondria are highly dynamic and can undergo biogenesis, fusion/fission, or autophagy. The transcription factor family, Kruppel-Like Factor (KLF), is necessary to carry out normal cellular processes from proliferation to differentiation. Recently, its importance in metabolic homeostasis in various tissue types has gained much attention. A handful of evidence supports KLF4’s involvement in regulating mitochondrial homeostasis in both healthy and cancer cells. In this review, we aim to summarize the available literature that demonstrates KLF4’s ability to modulate the mitochondrial life cycle in: Cardiac tissue, in which KLF4-knockdown subsequently leads to Heart Failure (HF), and Glioblastoma (GBM), where its expression promotes extensive mitochondrial fusion and offers mild cell protection under serum-deprivation. 2018-09-14 2018 /pmc/articles/PMC6594694/ /pubmed/31245170 http://dx.doi.org/10.4172/2157-7633.1000436 Text en http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Article
Tung, Brian
Xia, Shuli
Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title_full Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title_fullStr Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title_full_unstemmed Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title_short Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis
title_sort kruppel-like factor 4 (klf4) and its regulation on mitochondrial homeostasis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594694/
https://www.ncbi.nlm.nih.gov/pubmed/31245170
http://dx.doi.org/10.4172/2157-7633.1000436
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