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Role of renal tubular programed cell death in diabetic kidney disease

The pathogenic mechanism of diabetic kidney disease (DKD) is involved in various functions; however, its inadequate characterisation limits the availability of effective treatments. Tubular damage is closely correlated with renal function and is thought to be the main contributor to the injury obser...

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Detalles Bibliográficos
Autores principales: Zhou, Xiaojun, Xu, Chunmei, Dong, Jianjun, Liao, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10078574/
https://www.ncbi.nlm.nih.gov/pubmed/36401596
http://dx.doi.org/10.1002/dmrr.3596
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author Zhou, Xiaojun
Xu, Chunmei
Dong, Jianjun
Liao, Lin
author_facet Zhou, Xiaojun
Xu, Chunmei
Dong, Jianjun
Liao, Lin
author_sort Zhou, Xiaojun
collection PubMed
description The pathogenic mechanism of diabetic kidney disease (DKD) is involved in various functions; however, its inadequate characterisation limits the availability of effective treatments. Tubular damage is closely correlated with renal function and is thought to be the main contributor to the injury observed in early DKD. Programed cell death (PCD) occurs during the biological development of the living body. Accumulating evidence has clarified the fundamental role of abnormalities in tubular PCD during DKD pathogenesis. Among PCD types, classical apoptosis, autophagic cell death, and pyroptosis are the most studied and will be the focus of this review. Our review aims to elucidate the current knowledge of the mechanism of DKD and the potential therapeutic potential of drugs targeting tubular PCD pathways in DKD.
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spelling pubmed-100785742023-04-07 Role of renal tubular programed cell death in diabetic kidney disease Zhou, Xiaojun Xu, Chunmei Dong, Jianjun Liao, Lin Diabetes Metab Res Rev Review Article The pathogenic mechanism of diabetic kidney disease (DKD) is involved in various functions; however, its inadequate characterisation limits the availability of effective treatments. Tubular damage is closely correlated with renal function and is thought to be the main contributor to the injury observed in early DKD. Programed cell death (PCD) occurs during the biological development of the living body. Accumulating evidence has clarified the fundamental role of abnormalities in tubular PCD during DKD pathogenesis. Among PCD types, classical apoptosis, autophagic cell death, and pyroptosis are the most studied and will be the focus of this review. Our review aims to elucidate the current knowledge of the mechanism of DKD and the potential therapeutic potential of drugs targeting tubular PCD pathways in DKD. John Wiley and Sons Inc. 2022-11-30 2023-02 /pmc/articles/PMC10078574/ /pubmed/36401596 http://dx.doi.org/10.1002/dmrr.3596 Text en © 2022 The Authors. Diabetes/Metabolism Research and Reviews published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Review Article
Zhou, Xiaojun
Xu, Chunmei
Dong, Jianjun
Liao, Lin
Role of renal tubular programed cell death in diabetic kidney disease
title Role of renal tubular programed cell death in diabetic kidney disease
title_full Role of renal tubular programed cell death in diabetic kidney disease
title_fullStr Role of renal tubular programed cell death in diabetic kidney disease
title_full_unstemmed Role of renal tubular programed cell death in diabetic kidney disease
title_short Role of renal tubular programed cell death in diabetic kidney disease
title_sort role of renal tubular programed cell death in diabetic kidney disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10078574/
https://www.ncbi.nlm.nih.gov/pubmed/36401596
http://dx.doi.org/10.1002/dmrr.3596
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