Insights into the Molecular Mechanisms of NRF2 in Kidney Injury and Diseases DOI Open Access
Da-Wei Lin,

Yung‐Chien Hsu,

Cheng‐Chih Chang

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(7), P. 6053 - 6053

Published: March 23, 2023

Redox is a constant phenomenon in organisms. From the signaling pathway transduction to oxidative stress during inflammation and disease process, all are related reduction-oxidation (redox). Nuclear factor erythroid 2-related 2 (NRF2) transcription targeting many antioxidant genes. In non-stressed conditions, NRF2 maintains hemostasis of redox with housekeeping work. It expresses constitutively basal activity, maintained by Kelch-like-ECH-associated protein 1 (KEAP1)-associated ubiquitination degradation. When encountering stress, it can be up-regulated several mechanisms exert its anti-oxidative ability diseases or inflammatory processes protect tissues organs from further damage. acute kidney injury chronic diseases, such as diabetic nephropathy glomerular disease, results studies have suggested that, master regulating redox, therapeutic option. was not until early termination clinical phase 3 trial due heart failure an unexpected side effect that we renewed our understanding NRF2. just simple capacity but has pleiotropic activities, harmful helpful, depending on conditions backgrounds.

Language: Английский

Inflammation in obesity, diabetes, and related disorders DOI Creative Commons
Theresa V. Rohm, Daniel T. Meier, Jerrold M. Olefsky

et al.

Immunity, Journal Year: 2022, Volume and Issue: 55(1), P. 31 - 55

Published: Jan. 1, 2022

Language: Английский

Citations

1181
Macrophages: versatile players in renal inflammation and fibrosis DOI
Patrick Ming‐Kuen Tang, David J. Nikolic‐Paterson, Hui Y. Lan

et al.

Nature Reviews Nephrology, Journal Year: 2019, Volume and Issue: 15(3), P. 144 - 158

Published: Jan. 28, 2019

Language: Английский

Citations

767
Targeting innate immune mediators in type 1 and type 2 diabetes DOI
Marc Y. Donath, Charles A. Dinarello, Thomas Mandrup‐Poulsen

et al.

Nature reviews. Immunology, Journal Year: 2019, Volume and Issue: 19(12), P. 734 - 746

Published: Sept. 9, 2019

Language: Английский

Citations

336
Effects of SGLT2 inhibitors on systemic and tissue low-grade inflammation: The potential contribution to diabetes complications and cardiovascular disease DOI
Fabrice Bonnet, André Scheen

Diabetes & Metabolism, Journal Year: 2018, Volume and Issue: 44(6), P. 457 - 464

Published: Sept. 26, 2018

Language: Английский

Citations

265
Immune responses in diabetic nephropathy: Pathogenic mechanisms and therapeutic target DOI Creative Commons
Jiahao Chen, Qinhui Liu, Jinhan He

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Aug. 15, 2022

Diabetic nephropathy (DN) is a chronic, inflammatory disease affecting millions of diabetic patients worldwide. DN associated with proteinuria and progressive slowing glomerular filtration, which often leads to end-stage kidney diseases. Due the complexity this metabolic disorder lack clarity about its pathogenesis, it more difficult diagnose treat than other Recent studies have highlighted that immune system can inadvertently contribute pathogenesis. Cells involved in innate adaptive responses target due increased expression immune-related localization factors. Immune cells then activate pro-inflammatory response involving release autocrine paracrine factors, further amplify inflammation damage kidney. Consequently, strategies by targeting are currently under study. In light steady rise incidence, timely review summarizes latest findings role pathogenesis discusses promising preclinical clinical therapies.

Language: Английский

Citations

103
Identification and validation of immune and oxidative stress-related diagnostic markers for diabetic nephropathy by WGCNA and machine learning DOI Creative Commons
Mingming Xu, Hang Zhou, Ping Hu

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Feb. 22, 2023

Diabetic nephropathy (DN) is the primary cause of end-stage renal disease, but existing therapeutics are limited. Therefore, novel molecular pathways that contribute to DN therapy and diagnostics urgently needed.

Language: Английский

Citations

79
Renal macrophages and NLRP3 inflammasomes in kidney diseases and therapeutics DOI Creative Commons
Mohammad Islamuddin, Xuebin Qin

Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)

Published: May 13, 2024

Abstract Macrophages are exceptionally diversified cell types and perform unique features functions when exposed to different stimuli within the specific microenvironment of various kidney diseases. In instances tissue necrosis or infection, patterns associated with damage pathogens prompt development pro-inflammatory macrophages (M1). These M1 contribute exacerbating damage, inflammation, eventual fibrosis. Conversely, anti-inflammatory (M2) arise in same circumstances, contributing repair regeneration processes. Impaired causes fibrosis, hence play a protective pathogenic role. response harmful body, inflammasomes, complex assemblies multiple proteins, assume pivotal function innate immunity. The initiation inflammasomes triggers activation caspase 1, which turn facilitates maturation cytokines, death. kidneys possess complete elements NLRP3 inflammasome, including NLRP3, ASC, pro-caspase-1. When activated, it caspase-1, resulting release mature proinflammatory cytokines (IL)-1β IL-18 cleavage Gasdermin D (GSDMD). This process therefore then induces pyroptosis, leading renal death, dysfunction. NLRP3–ASC–caspase-1–IL-1β–IL-18 pathway has been identified as factor pathophysiology numerous this review, we explore current progress understanding macrophage behavior concerning injury, fibrosis kidneys. Emphasizing role activated both advancement recovery phases diseases, article delves into potential strategies modify functionality also discusses emerging approaches selectively target their signaling components kidney, aiming facilitate healing

Language: Английский

Citations

22
Diabetic gut microbiota dysbiosis as an inflammaging and immunosenescence condition that fosters progression of retinopathy and nephropathy DOI Creative Commons
Rosa Fernandes, Sofia Viana, Sara Nunes

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2018, Volume and Issue: 1865(7), P. 1876 - 1897

Published: Oct. 1, 2018

Language: Английский

Citations

141
Tim-3 aggravates podocyte injury in diabetic nephropathy by promoting macrophage activation via the NF-κB/TNF-α pathway DOI Creative Commons
Huimin Yang, Tingting Xie,

Dengren Li

et al.

Molecular Metabolism, Journal Year: 2019, Volume and Issue: 23, P. 24 - 36

Published: Feb. 26, 2019

Macrophage-mediated inflammation plays a significant role in the development and progression of diabetic nephropathy (DN). However, underlying mechanisms remain unclear. Studies suggest that T cell immunoglobulin domain mucin domain-3 (Tim-3) has complicated roles regulating macrophage activation, but its DN are still completely unknown.We downregulated Tim-3 expression kidney (intrarenal injection shRNA expressing lentivirus or global knockout mice) induced by streptozotocin (STZ). We analyzed degree renal injury, especially podocyte injury activated macrophages vitro vivo. Then, we transferred different bone marrow derived (BMs) into STZ-induced knockdown mice to examine effects on DN.First, found was increased patients with two mouse models, i.e. db/db mice, positively correlated dysfunction patients. deficiency ameliorated damage diabetes concurrent increase protein levels Nephrin WT-1. Similar were observed mice. Second, adoptive transfer Tim-3-expressing macrophages, not accelerated suggesting key for DN. Furthermore, NF-κB activation TNF-α excretion upregulated kidneys, associated Tim-3-mediated NF-κB/TNF-α signaling pathway both vivo vitro.These results functions as regulator inflammatory processes serves potential therapeutic target

Language: Английский

Citations

139
Protective effect of ginsenoside metabolite compound K against diabetic nephropathy by inhibiting NLRP3 inflammasome activation and NF-κB/p38 signaling pathway in high-fat diet/streptozotocin-induced diabetic mice DOI
Song Wu, Lin Wei,

Yanwei Du

et al.

International Immunopharmacology, Journal Year: 2018, Volume and Issue: 63, P. 227 - 238

Published: Aug. 11, 2018

Language: Английский

Citations

124