ArticleScientific reports2019
Angiotensin II-mediated MYH9 downregulation causes structural and functional podocyte injury in diabetic kidney disease.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
- Chronic stress disrupts the network among stress granules, P-bodies, and motor proteins.bioRxiv : the preprint server for biology · 2026Article
- Upregulation of angiotensin-(1-7) formation in human podocytes - enzyme activity assay upon fluid flow shear stress.PloS one · 2026Article
- Spexin peptide ameliorates renal injury in diabetic nephropathy rat model via modulation of metabolic, oxidative, inflammatory, and apoptotic dysregulations.Journal of physiology and biochemistry · 2025Article
- Role of myosin heavy chain 9 in gastrointestinal tumorigenesis: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
- TUBB4A relieves high glucose-induced cardiomyocyte hypertrophy and apoptosis through the regulation of ubiquitination and activation of the NOTCH signaling pathway.Cytotechnology · 2025Article
- Functional Microendoscopy Reveals Calcium Responses of Single Cells in Tracheal Tuft Cells and Kidney Podocytes.Small (Weinheim an der Bergstrasse, Germany) · 2025Article
- Nephroprotective Effects ofCurrent issues in molecular biology · 2025Article
- Endothelial FOSL1 drives angiotensin II-induced myocardial injury via AT1R-upregulated MYH9.Acta pharmacologica Sinica · 2025Article
- MYH9-related disease with a normal platelet count.CEN case reports · 2025Article
- Human congenital cataract mutation inInternational journal of ophthalmology · 2025Article
- Celastrol protects against diabetic nephropathy by modulating immune-related pathways: a bioinformatics and experimental validation.American journal of translational research · 2025Article
- Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Quantitative Proteomics Combined with Network Pharmacology Analysis Unveils the Biological Basis of Schisandrin B in Treating Diabetic Nephropathy.Combinatorial chemistry & high throughput screening · 2024Article
- PFKFB3 downregulation aggravates Angiotensin II-induced podocyte detachment.Renal failure · 2023Article
- Plasma-Derived Exosome Proteins as Novel Diagnostic and Prognostic Biomarkers in Neuroblastoma Patients.Cells · 2023Article
- Pediatric Type 1 Diabetes: Mechanisms and Impact of Technologies on Comorbidities and Life Expectancy.International journal of molecular sciences · 2023Review
- Oxidative stress and inflammation in diabetic nephropathy: role of polyphenols.Frontiers in immunology · 2023Review
- Sestrin2 Signaling Pathway Regulates Podocyte Biology and Protects against Diabetic Nephropathy.Journal of diabetes research · 2023Review
- Hepatic and proximal tubule angiotensinogen play distinct roles in kidney dysfunction, glomerular and tubular injury, and fibrosis progression.American journal of physiology. Renal physiology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYH9, a widely expressed gene encoding nonmuscle myosin heavy chain, is also expressed in podocytes and is associated with glomerular pathophysiology. However, the mechanisms underlying MYH9-related glomerular diseases associated with proteinuria are poorly understood. Therefore, we investigated the role and mechanism of MYH9 in diabetic kidney injury. MYH9 expression was decreased in glomeruli from diabetic patients and animals and in podocytes treated with Ang II in vitro. Ang II treatment and siRNA-mediated MYH9 knockdown in podocytes resulted in actin cytoskeleton reorganization, reduced cell adhesion, actin-associated protein downregulation, and increased albumin permeability. Ang II treatment increased NOX4 expression and ROS generation. The Ang II receptor blocker losartan and the ROS scavenger NAC restored MYH9 expression in Ang II-treated podocytes, attenuated disrupted actin cytoskeleton and decreased albumin permeability. Furthermore, MYH9 overexpression in podocytes restored the effects of Ang II on the actin cytoskeleton and actin-associated proteins. Ang II-mediated TRPC6 activation reduced MYH9 expression. These results suggest that Ang II-mediated MYH9 depletion in diabetic nephropathy may increase filtration barrier permeability by inducing structural and functional podocyte injury through TRPC6-mediated Ca
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