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Optical Angiography at Diabetes
Published in Andrey V. Dunaev, Valery V. Tuchin, Biomedical Photonics for Diabetes Research, 2023
Dan Zhu, Jingtan Zhu, Dongyu Li, Tingting Yu, Wei Feng, Rui Shi
Hasegawa et al. utilized T1D rat and mouse models induced by STZ or alloxan and CUBIC-kidney clearing protocol to clarify the net effects of HIF stabilization on energy metabolism in diabetic kidney [12]. They also performed comprehensive 3D analysis to visualize glomeruli in the kidney using anti-podocin antibodies. They found that renal pathological abnormalities (glomerulomegaly and GBM thickening) induced by diabetes in the early stages of DN could be mitigated by enarodustat treatment.
Potential of Fenugreek in Management of Kidney and Lung Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Amit D. Kandhare, Anwesha A. Mukherjee-Kandhare, Subhash L. Bodhankar
A study demonstrated the potential of dietary fenugreek seed (3%) administration against renin-angiotensin system-mediated renal damage in diabetic rats (Pradeep, Barman, and Srinivasan 2019). Fenugreek seed administration showed profound down-regulation in renal glucose transporters (GLUT-1 and GLUT-2), renal angiotensin-converting enzyme (ACE activity) and AT1 receptor expression, metabolites of the polyol pathway, and N-acetyl-β-d-glycosaminidase activity. The upregulated expression of kidney injury molecule-1, inducible nitric oxide, and type I collagen were markedly ameliorated by dietary fenugreek. Furthermore, podocyte damage was partially restored by fenugreek administration reflected by a correction in urinary nephrin, podocin, and podocalyxin markers. Diabetes-induced renal aberrations were also reduced by dietary fenugreek intake. The researcher concluded that dietary intake of fiber-rich fenugreek seeds was associated with inhibition of glucose translocation and renin-angiotensin system, which halted the development of diabetic nephropathy (Pradeep, Barman, and Srinivasan 2019).
Combination therapy with DHA and BMSCs suppressed podocyte injury and attenuated renal fibrosis by modulating the TGF-β1/Smad pathway in MN mice
Published in Renal Failure, 2023
Yongzhang Li, Suzhi Chen, Jinchuan Tan, Yan Zhou, Meifang Ren, Qian Zhang, Meijiao Zhao, Guodong Yuan, Wenxi Zhang, Fengwen Yang
Podocytes are terminally differentiated cells in the glomerulus with regularly spaced foot processes that control glomerular filtration via the slit diaphragm [30]. Persistent podocyte injury results in podocyte loss and death, leading to progressive kidney damage and ultimately kidney failure [31]. Indeed, podocyte injury enhanced the increase in proteinuria; as a result, podocytes are believed to be the primary target of MN. Podocin and nephrin are the main components of the slit diaphragm, which play key roles in maintaining filtration barrier integrity [32]. In the present study, we found that combination therapy with DHA and BMSCs decreased the expression of podocin and nephrin. These results suggested that combination therapy with DHA and BMSCs has the potential to protect podocytes during kidney injury.
TNF-α-mediated podocyte injury via the apoptotic death receptor pathway in a mouse model of IgA nephropathy
Published in Renal Failure, 2022
Qiang Wan, Jiabao Zhou, Yansheng Wu, Liqiang Shi, Weiwei Liu, Jiaoying Ou, Jiandong Gao
Podocytes, the GBM and endothelial cells constitute the glomerular filtration membrane, and the foot processes of neighboring podocytes are interdigitated, forming a complex modified adherens junction, known as the slit diaphragm [6]. Podocyte injury involves apoptosis, necrosis, detachment from the GBM and defective autophagy, ultimately leading to proteinuria [25]. The reduction in the number of podocytes in IgAN is closely associated with disease severity [26]. In vitro experiments have revealed that the mesangial cell-derived humoral factor TNF-α can alter glomerular permeability and cause podocyte apoptosis in the event of proteinuria in IgAN [7]. Nephrin is an important podocyte-specific protein and it is involved in signaling pathways regulating actin dynamics and cell survival [27]. Podocin is a structural molecule that interacts with nephrin and they both play an important role in supporting the slit diaphragm [28,29]. However, the pathway and underlying mechanisms through which TNF-α leads to podocyte apoptosis in IgAN have yet to be fully elucidated.
Kidney and lipids: novel potential therapeutic targets for dyslipidemia in kidney disease?
Published in Expert Opinion on Therapeutic Targets, 2022
Konrad Zuzda, Wiktoria Grycuk, Jacek Małyszko, Jolanta Małyszko
Lipid raft-like microdomains are involved in the spatial organization of the slit diaphragm [86]. Enriched with cholesterol, glycosphingolipids, and multiple signaling molecules, the lipid rafts regulate vital cellular processes such as intercellular signaling adhesion, or endocytosis [86,87]. Changes in raft proteome localization can be attributed to changes in cholesterol level [88]. In mouse macrophages, lipid raft levels and the signaling potential of TLR4 are associated with cholesterol levels [89]. It has been suggested that cholesterol is required for podocin function [90]. Podocin is part of a transmembrane complex responsible for the cytoskeletal rearrangement and transcriptional activity in podocytes [91,92]. NPHS2, which encodes podocin, is mutated in a subset of familial steroid-resistant nephrotic syndrome [93]. Together, the proteins that form the podocin complex, including nephrin and transient receptor potential C channel (TRPC6), facilitate signal transduction [91,92,94]. Huber et al. [90] found that cholesterol binding to podocin is essential for TRPC6 ion channel activity, and therefore, the regulation of intracellular processes.