Cargando…

Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury

Acute kidney injury (AKI) induces significant energy metabolic reprogramming in renal tubular epithelial cells (TECs), thereby altering lipid, glucose, and amino acid metabolism. The changes in lipid metabolism encompass not only the downregulation of fatty acid oxidation (FAO) but also changes in c...

Descripción completa

Detalles Bibliográficos
Autores principales: Zhao, Limei, Hao, Yajie, Tang, Shuqin, Han, Xiutao, Li, Rongshan, Zhou, Xiaoshuang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10694365/
http://dx.doi.org/10.3389/fcell.2023.1276217
_version_ 1785153360452648960
author Zhao, Limei
Hao, Yajie
Tang, Shuqin
Han, Xiutao
Li, Rongshan
Zhou, Xiaoshuang
author_facet Zhao, Limei
Hao, Yajie
Tang, Shuqin
Han, Xiutao
Li, Rongshan
Zhou, Xiaoshuang
author_sort Zhao, Limei
collection PubMed
description Acute kidney injury (AKI) induces significant energy metabolic reprogramming in renal tubular epithelial cells (TECs), thereby altering lipid, glucose, and amino acid metabolism. The changes in lipid metabolism encompass not only the downregulation of fatty acid oxidation (FAO) but also changes in cell membrane lipids and triglycerides metabolism. Regarding glucose metabolism, AKI leads to increased glycolysis, activation of the pentose phosphate pathway (PPP), inhibition of gluconeogenesis, and upregulation of the polyol pathway. Research indicates that inhibiting glycolysis, promoting the PPP, and blocking the polyol pathway exhibit a protective effect on AKI-affected kidneys. Additionally, changes in amino acid metabolism, including branched-chain amino acids, glutamine, arginine, and tryptophan, play an important role in AKI progression. These metabolic changes are closely related to the programmed cell death of renal TECs, involving autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis. Notably, abnormal intracellular lipid accumulation can impede autophagic clearance, further exacerbating lipid accumulation and compromising autophagic function, forming a vicious cycle. Recent studies have demonstrated the potential of ameliorating AKI-induced kidney damage through calorie and dietary restriction. Consequently, modifying the energy metabolism of renal TECs and dietary patterns may be an effective strategy for AKI treatment.
format Online
Article
Text
id pubmed-10694365
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-106943652023-12-05 Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury Zhao, Limei Hao, Yajie Tang, Shuqin Han, Xiutao Li, Rongshan Zhou, Xiaoshuang Front Cell Dev Biol Cell and Developmental Biology Acute kidney injury (AKI) induces significant energy metabolic reprogramming in renal tubular epithelial cells (TECs), thereby altering lipid, glucose, and amino acid metabolism. The changes in lipid metabolism encompass not only the downregulation of fatty acid oxidation (FAO) but also changes in cell membrane lipids and triglycerides metabolism. Regarding glucose metabolism, AKI leads to increased glycolysis, activation of the pentose phosphate pathway (PPP), inhibition of gluconeogenesis, and upregulation of the polyol pathway. Research indicates that inhibiting glycolysis, promoting the PPP, and blocking the polyol pathway exhibit a protective effect on AKI-affected kidneys. Additionally, changes in amino acid metabolism, including branched-chain amino acids, glutamine, arginine, and tryptophan, play an important role in AKI progression. These metabolic changes are closely related to the programmed cell death of renal TECs, involving autophagy, apoptosis, necroptosis, pyroptosis, and ferroptosis. Notably, abnormal intracellular lipid accumulation can impede autophagic clearance, further exacerbating lipid accumulation and compromising autophagic function, forming a vicious cycle. Recent studies have demonstrated the potential of ameliorating AKI-induced kidney damage through calorie and dietary restriction. Consequently, modifying the energy metabolism of renal TECs and dietary patterns may be an effective strategy for AKI treatment. Frontiers Media S.A. 2023-11-20 /pmc/articles/PMC10694365/ http://dx.doi.org/10.3389/fcell.2023.1276217 Text en Copyright © 2023 Zhao, Hao, Tang, Han, Li 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
Zhao, Limei
Hao, Yajie
Tang, Shuqin
Han, Xiutao
Li, Rongshan
Zhou, Xiaoshuang
Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title_full Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title_fullStr Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title_full_unstemmed Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title_short Energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
title_sort energy metabolic reprogramming regulates programmed cell death of renal tubular epithelial cells and might serve as a new therapeutic target for acute kidney injury
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10694365/
http://dx.doi.org/10.3389/fcell.2023.1276217
work_keys_str_mv AT zhaolimei energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury
AT haoyajie energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury
AT tangshuqin energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury
AT hanxiutao energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury
AT lirongshan energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury
AT zhouxiaoshuang energymetabolicreprogrammingregulatesprogrammedcelldeathofrenaltubularepithelialcellsandmightserveasanewtherapeutictargetforacutekidneyinjury