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Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms

Diabetic kidney disease (DKD) is a serious complication of diabetes that can lead to end-stage kidney disease. Despite its significant impact, most research has concentrated on the glomerulus, with little attention paid to the tubulointerstitial region, which accounts for the majority of the kidney...

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Autores principales: Xu, Chengren, Ha, Xiaowen, Yang, Shufen, Tian, Xuefei, Jiang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10583558/
https://www.ncbi.nlm.nih.gov/pubmed/37859992
http://dx.doi.org/10.3389/fendo.2023.1232790
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author Xu, Chengren
Ha, Xiaowen
Yang, Shufen
Tian, Xuefei
Jiang, Hong
author_facet Xu, Chengren
Ha, Xiaowen
Yang, Shufen
Tian, Xuefei
Jiang, Hong
author_sort Xu, Chengren
collection PubMed
description Diabetic kidney disease (DKD) is a serious complication of diabetes that can lead to end-stage kidney disease. Despite its significant impact, most research has concentrated on the glomerulus, with little attention paid to the tubulointerstitial region, which accounts for the majority of the kidney volume. DKD’s tubulointerstitial lesions are characterized by inflammation, fibrosis, and loss of kidney function, and recent studies indicate that these lesions may occur earlier than glomerular lesions. Evidence has shown that inflammatory mechanisms in the tubulointerstitium play a critical role in the development and progression of these lesions. Apart from the renin-angiotensin-aldosterone blockade, Sodium-Glucose Linked Transporter-2(SGLT-2) inhibitors and new types of mineralocorticoid receptor antagonists have emerged as effective ways to treat DKD. Moreover, researchers have proposed potential targeted therapies, such as inhibiting pro-inflammatory cytokines and modulating T cells and macrophages, among others. These therapies have demonstrated promising results in preclinical studies and clinical trials, suggesting their potential to treat DKD-induced tubulointerstitial lesions effectively. Understanding the immune-inflammatory mechanisms underlying DKD-induced tubulointerstitial lesions and developing targeted therapies could significantly improve the treatment and management of DKD. This review summarizes the latest advances in this field, highlighting the importance of focusing on tubulointerstitial inflammation mechanisms to improve DKD outcomes.
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spelling pubmed-105835582023-10-19 Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms Xu, Chengren Ha, Xiaowen Yang, Shufen Tian, Xuefei Jiang, Hong Front Endocrinol (Lausanne) Endocrinology Diabetic kidney disease (DKD) is a serious complication of diabetes that can lead to end-stage kidney disease. Despite its significant impact, most research has concentrated on the glomerulus, with little attention paid to the tubulointerstitial region, which accounts for the majority of the kidney volume. DKD’s tubulointerstitial lesions are characterized by inflammation, fibrosis, and loss of kidney function, and recent studies indicate that these lesions may occur earlier than glomerular lesions. Evidence has shown that inflammatory mechanisms in the tubulointerstitium play a critical role in the development and progression of these lesions. Apart from the renin-angiotensin-aldosterone blockade, Sodium-Glucose Linked Transporter-2(SGLT-2) inhibitors and new types of mineralocorticoid receptor antagonists have emerged as effective ways to treat DKD. Moreover, researchers have proposed potential targeted therapies, such as inhibiting pro-inflammatory cytokines and modulating T cells and macrophages, among others. These therapies have demonstrated promising results in preclinical studies and clinical trials, suggesting their potential to treat DKD-induced tubulointerstitial lesions effectively. Understanding the immune-inflammatory mechanisms underlying DKD-induced tubulointerstitial lesions and developing targeted therapies could significantly improve the treatment and management of DKD. This review summarizes the latest advances in this field, highlighting the importance of focusing on tubulointerstitial inflammation mechanisms to improve DKD outcomes. Frontiers Media S.A. 2023-10-04 /pmc/articles/PMC10583558/ /pubmed/37859992 http://dx.doi.org/10.3389/fendo.2023.1232790 Text en Copyright © 2023 Xu, Ha, Yang, Tian and Jiang 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 Endocrinology
Xu, Chengren
Ha, Xiaowen
Yang, Shufen
Tian, Xuefei
Jiang, Hong
Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title_full Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title_fullStr Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title_full_unstemmed Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title_short Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
title_sort advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10583558/
https://www.ncbi.nlm.nih.gov/pubmed/37859992
http://dx.doi.org/10.3389/fendo.2023.1232790
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