ArticleNephrology (Carlton, Vic.)2024
Heat shock protein 70 promotes the progression of type 2 diabetic nephropathy by inhibiting T-cell immunoglobulin and mucin domain-3 and thereby promoting Th17/Treg imbalance.
Article in Nephrology (Carlton, Vic.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- CD4Frontiers in immunology · 2026Review
- Single-Cell Maps Reveal Novel Mechanisms of Ferroptosis and Biomarkers in Diabetic Nephropathy.Current medicinal chemistry · 2026Article
- Gut Microbiota Dysbiosis and Metabolite Imbalance Mediate Diabetic Kidney Disease Inflammation: Mechanisms and Intervention Strategies Targeting Gut-Kidney Axis and NF-κB/NLRP3 Pathways.Journal of inflammation research · 2026Review
- Association of increased serum I-309 with renal function impairment and diabetic kidney disease in type 2 diabetes mellitus.Endocrine connections · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
aimDiabetic nephropathy (DN) is the most common complication of diabetes mellitus. We aimed to investigate the role of regulatory T cells (Tregs) and helper T cells 17 (Th17) in the development and progression of DN.
methodsA mouse type 2 diabetic nephropathy (T2DN) model was established. Immunohistochemistry was used to detect the expression of HSP70 and Tim-3 in mouse kidney tissues, and western blotting was used to detect the expression levels of HSP70 and Tim-3. PAS staining and Masson's trichrome staining were used to detect the degree of kidney injury. Flow cytometry was used to detect the number of Th17 and Treg cells in blood and kidney tissues. The expression levels of interleukin 17 (IL-17) and interleukin 10 (IL-10) in the serum were measured via ELISA.
resultsThe expression of HSP70 was significantly increased while the expression of Tim-3 was significantly decreased in the kidneys of mice in the T2DN group compared with those in the control (NC) group. Additionally, the inhibition of HSP70 upregulated the expression of Tim-3 in T2DN mice. The Th17/Treg ratio was significantly greater in the blood and kidneys of the mice in the T2DN group than in those of the NC group, the expression of serum IL-17 was increased, and the expression of IL-10 was decreased.
conclusionIncreased HSP70 inhibits Tim-3 expression in T2DN mouse kidney tissues, and subsequently causes a Th17/Treg imbalance and an inflammatory response, ultimately leading to kidney injury. The inhibition of HSP70 may alleviate the progression of T2DN.
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