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Organelle Stress and Metabolic Derangement in Kidney Disease

Advanced multiomics analysis has revealed novel pathophysiological mechanisms in kidney disease. In particular, proteomic and metabolomic analysis shed light on mitochondrial dysfunction (mitochondrial stress) by glycation in diabetic or age-related kidney disease. Further, metabolic damage often re...

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Detalles Bibliográficos
Autor principal: Inagi, Reiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836232/
https://www.ncbi.nlm.nih.gov/pubmed/35163648
http://dx.doi.org/10.3390/ijms23031723
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author Inagi, Reiko
author_facet Inagi, Reiko
author_sort Inagi, Reiko
collection PubMed
description Advanced multiomics analysis has revealed novel pathophysiological mechanisms in kidney disease. In particular, proteomic and metabolomic analysis shed light on mitochondrial dysfunction (mitochondrial stress) by glycation in diabetic or age-related kidney disease. Further, metabolic damage often results from organelle stress, such as mitochondrial stress and endoplasmic reticulum (ER) stress, as well as interorganelle communication, or “organelle crosstalk”, in various kidney cells. These contribute to progression of the disease phenotype. Aberrant tubular mitochondrial lipid metabolism leads to tubular inflammation and fibrosis. This review article summarizes updated evidence regarding organelle stress, organelle crosstalk, and metabolic derangement in kidney disease.
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spelling pubmed-88362322022-02-12 Organelle Stress and Metabolic Derangement in Kidney Disease Inagi, Reiko Int J Mol Sci Review Advanced multiomics analysis has revealed novel pathophysiological mechanisms in kidney disease. In particular, proteomic and metabolomic analysis shed light on mitochondrial dysfunction (mitochondrial stress) by glycation in diabetic or age-related kidney disease. Further, metabolic damage often results from organelle stress, such as mitochondrial stress and endoplasmic reticulum (ER) stress, as well as interorganelle communication, or “organelle crosstalk”, in various kidney cells. These contribute to progression of the disease phenotype. Aberrant tubular mitochondrial lipid metabolism leads to tubular inflammation and fibrosis. This review article summarizes updated evidence regarding organelle stress, organelle crosstalk, and metabolic derangement in kidney disease. MDPI 2022-02-02 /pmc/articles/PMC8836232/ /pubmed/35163648 http://dx.doi.org/10.3390/ijms23031723 Text en © 2022 by the author. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Inagi, Reiko
Organelle Stress and Metabolic Derangement in Kidney Disease
title Organelle Stress and Metabolic Derangement in Kidney Disease
title_full Organelle Stress and Metabolic Derangement in Kidney Disease
title_fullStr Organelle Stress and Metabolic Derangement in Kidney Disease
title_full_unstemmed Organelle Stress and Metabolic Derangement in Kidney Disease
title_short Organelle Stress and Metabolic Derangement in Kidney Disease
title_sort organelle stress and metabolic derangement in kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8836232/
https://www.ncbi.nlm.nih.gov/pubmed/35163648
http://dx.doi.org/10.3390/ijms23031723
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