Oś MIF/CD74 jako cel terapii metforminą w podocytopatii cukrzycowej — rzeczywista praktyka kliniczna

Xing, Yan; Ye, Shandong; Chen, Yan; Fan, Aihong; Zhao, Xu; Jiang, Wei

doi:10.5603/ep.a2018.0028

Cited by 6 publications

(2 citation statements)

References 27 publications

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“…The authors conclude that metformin reduces the inflammatory signaling by MIF-CD74 in podocytes and could, thus, protect the podocytes from injury. This effect of metformin is independent of the glycemic control because there were no differences in the fasting blood glucose of HbA1c values between the examined groups [158]. This can confirm that metformin has an anti-inflammatory effect but it should be checked in a larger study with modern antidiabetic drugs.…”

Section: Impact Of Metformin On Inflammation and Fibrosis In Dkdmentioning

confidence: 54%

Insight into the Molecular Mechanism of Diabetic Kidney Disease and the Role of Metformin in Its Pathogenesis

Kleibert,

Zygmunciak,

Łakomska

et al. 2023

IJMS

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Diabetic kidney disease (DKD) is one of the leading causes of death among patients diagnosed with diabetes mellitus. Despite the growing knowledge about the pathogenesis of DKD, we still do not have effective direct pharmacotherapy. Accurate blood sugar control is essential in slowing down DKD. It seems that metformin has a positive impact on kidneys and this effect is not only mediated by its hypoglycemic action, but also by direct molecular regulation of pathways involved in DKD. The molecular mechanism of DKD is complex and we can distinguish polyol, hexosamine, PKC, and AGE pathways which play key roles in the development and progression of this disease. Each of these pathways is overactivated in a hyperglycemic environment and it seems that most of them may be regulated by metformin. In this article, we summarize the knowledge about DKD pathogenesis and the potential mechanism of the nephroprotective effect of metformin. Additionally, we describe the impact of metformin on glomerular endothelial cells and podocytes, which are harmed in DKD.

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Section: Impact Of Metformin On Inflammation and Fibrosis In Dkdmentioning

confidence: 54%

Insight into the Molecular Mechanism of Diabetic Kidney Disease and the Role of Metformin in Its Pathogenesis

Kleibert,

Zygmunciak,

Łakomska

et al. 2023

IJMS

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“…Metformin showed its podocyte-protective capacity in type 2 diabetic patients, and the underlying mechanisms might be partly attributable to its effects on the M1 polarization-related MIF-CD74 axis [ 39 , 40 ]. Further exploratory studies on the protective effects of Tha on podocyte via modulation of the balance between the M1/M2 phenotype should be conducted in DKD animal models.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation

Liao

Zhang

et al. 2020

Journal of Immunology Research

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Objective. It has been shown that podocyte injury represents an important pathological basis that contributes to proteinuria and eventually leads to kidney failure. High glucose (HG) activates macrophage polarization, further exacerbating HG-induced podocyte injury. Our previous study on diabetic nephropathy rats indicated that thalidomide (Tha) has renoprotective properties. The present study explored the effects of Tha on mRNA and protein expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor- (TNF-) α, mannose receptor (CD206), and arginase- (Arg-) 1 in HG-activated macrophages. iNOS and TNF-α are established as markers of classically activated macrophage (M1). CD206 and Arg-1 are regarded as markers of alternatively activated macrophages (M2). During the experiment, the supernatants of (HG)-treated and (Tha)-treated macrophages, designated as (HG) MS and (Tha) MS, were simultaneously collected and processed. TNF-α and interleukin- (IL-) 1β levels as well as protein expressions of nephrin and podocin in HG, (HG) MS, and (Tha) MS-cultured podocytes were evaluated. The results showed that compared to the 11.1 mM normal glucose (NG), the 33.3 mM HG-cultured RAW 264.7 cells exhibited upregulated iNOS and TNF-α mRNAs and protein expressions, and downregulated CD206 and Arg-1 expressions significantly (p<0.05). Tha 200 μg/ml suppressed iNOS and TNF-α, and promoted CD206 and Arg-1 expressions significantly compared to the HG group (p<0.05). Furthermore, (HG) MS-treated podocytes showed an increase in TNF-α and IL-1β levels and a downregulation in nephrin and podocin expression significantly compared to NG-treated and HG-treated podocytes (p<0.05). The (Tha 200 μg/ml) MS group exhibited a decrease in TNF-α and IL-1β level, and an upregulation in nephrin and podocin expressions significantly compared to the (HG) MS group (p<0.05). Our research confirmed that HG-activated macrophage differentiation aggravates HG-induced podocyte injury in vitro and the protective effects of Tha might be related to its actions on TNF-α and IL-1β levels via its modulation on M1/M2 differentiation.

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Protection by metformin against severe Covid-19: An in-depth mechanistic analysis

Wiernsperger

Al‐Salameh

Cariou

et al. 2022

Diabetes & Metabolism

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Oś MIF/CD74 jako cel terapii metforminą w podocytopatii cukrzycowej — rzeczywista praktyka kliniczna

Abstract: Metformin could present its podocyte-protective capacity in type 2 diabetics and the underlying mechanisms may be partly attributed to its effects in suppressing MIF-CD74 axis mediated inflammatory cascade response. < p > < /p >.

Cited by 6 publications

References 27 publications

Insight into the Molecular Mechanism of Diabetic Kidney Disease and the Role of Metformin in Its Pathogenesis

Insight into the Molecular Mechanism of Diabetic Kidney Disease and the Role of Metformin in Its Pathogenesis

Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation

Protection by metformin against severe Covid-19: An in-depth mechanistic analysis

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