ArticleNature communications2022
Simultaneous stabilization of actin cytoskeleton in multiple nephron-specific cells protects the kidney from diverse injury.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- New potential therapeutic targets of metabolic disorder-associated kidney disease and diabetic kidney disease.Kidney international · 2026Review
- The association between endothelial activation and stress Index and the development and prognosis of acute kidney injury in elderly patients with critical illness.Renal failure · 2025Article
- Rac1 promotes proximal tubule kidney repair by coupling the actin cytoskeleton to mitochondrial function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Integrins in the kidney - beyond the matrix.Nature reviews. Nephrology · 2025Review
- Cytoskeleton Rearrangement Decreases Mitochondrial Fatty Acid Oxidation in Renal Tubular Epithelial Cells Contributing to Renal Fibrogenesis.Drug design, development and therapy · 2025Article
- Designer peptide-DNA cytoskeletons regulate the function of synthetic cells.Nature chemistry · 2024Article
- Evaluation of a proteomic signature coupled with the kidney failure risk equation in predicting end stage kidney disease in a chronic kidney disease cohort.Clinical proteomics · 2024Article
- Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.Science advances · 2024Article
- Modeled microgravity unravels the roles of mechanical forces in renal progenitor cell physiology.Stem cell research & therapy · 2024Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Effects of DJ‑1 on apoptosis and mitophagy of glomerular podocytes.Experimental and therapeutic medicine · 2023Article
- Is Renal Ischemic Preconditioning an Alternative to Ameliorate the Short- and Long-Term Consequences of Acute Kidney Injury?International journal of molecular sciences · 2023Review
- Moonlighting chromatin: when DNA escapes nuclear control.Cell death and differentiation · 2023Review
- Network pharmacology and molecular docking of endogenous active metabolites in diabetic kidney disease.Renal failure · 2023Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Chronic kidney diseases and acute kidney injury are mechanistically distinct kidney diseases. While chronic kidney diseases are associated with podocyte injury, acute kidney injury affects renal tubular epithelial cells. Despite these differences, a cardinal feature of both acute and chronic kidney diseases is dysregulated actin cytoskeleton. We have shown that pharmacological activation of GTPase dynamin ameliorates podocyte injury in murine models of chronic kidney diseases by promoting actin polymerization. Here we establish dynamin's role in modulating stiffness and polarity of renal tubular epithelial cells by crosslinking actin filaments into branched networks. Activation of dynamin's crosslinking capability by a small molecule agonist stabilizes the actomyosin cortex of the apical membrane against injury, which in turn preserves renal function in various murine models of acute kidney injury. Notably, a dynamin agonist simultaneously attenuates podocyte and tubular injury in the genetic murine model of Alport syndrome. Our study provides evidence for the feasibility and highlights the benefits of novel holistic nephron-protective therapies.
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