ArticlePloS one2013
Activation of Rac-1 and RhoA contributes to podocyte injury in chronic kidney disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 90 citations in OpenAlex.
- ELMO1 dependent efferocytosis protects from nephrotoxin induced acute kidney injury.Cell death discovery · 2026Article
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- Simvastatin Mitigates Kidney Injury via Inhibition of the TNF-α/α-SMA Signaling Pathway in a Subtotal Nephrectomy Model.Journal of experimental pharmacology · 2026Article
- Immune mechanisms and immunomodulatory therapies in steroid-resistant nephrotic syndrome.Renal failure · 2025Review
- Interplay Between the Mineralocorticoid System, Inflammation, Hypertension, and Kidney Disease.Kidney360 · 2025Review
- Mechanisms of podocyte injury in genetic kidney disease.Pediatric nephrology (Berlin, Germany) · 2025Review
- Migrasomes as intercellular messengers: potential in the pathological mechanism, diagnosis and treatment of clinical diseases.Journal of nanobiotechnology · 2025Review
- Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025Review
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- The Protective Effects of Vitamin B Complex on Diclofenac Sodium-Induced Nephrotoxicity: The Role of NOX4/RhoA/ROCK.Inflammation · 2024Article
- Role of biophysics and mechanobiology in podocyte physiology.Nature reviews. Nephrology · 2024Review
- 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
- Effects of a High-Protein Diet on Kidney Injury under Conditions of Non-CKD or CKD in Mice.International journal of molecular sciences · 2023Article
- Transmembrane signaling molecules play a key role in the pathogenesis of IgA nephropathy: a weighted gene co-expression network analysis study.BMC immunology · 2021Article
- A novel approach to identify the mechanism of miR-145-5p toxicity to podocytes based on the essential genes targeting analysis.Molecular therapy. Nucleic acids · 2021Article
- Role of actin cytoskeleton in podocytes.Pediatric nephrology (Berlin, Germany) · 2021Review
- Islet Transplantation Reverses Podocyte Injury in Diabetic Nephropathy or Induced by High Glucose via Inhibiting RhoA/ROCK/NF-Journal of diabetes research · 2021Article
- Podocyte-Released Migrasomes in Urine Serve as an Indicator for Early Podocyte Injury.Kidney diseases (Basel, Switzerland) · 2020Article
- The potential roles of NAD(P)H:quinone oxidoreductase 1 in the development of diabetic nephropathy and actin polymerization.Scientific reports · 2020Article
- Surface coating determines the inflammatory potential of magnetite nanoparticles in murine renal podocytes and mesangial cells.RSC advances · 2020Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rho-family GTPases like RhoA and Rac-1 are potent regulators of cellular signaling that control gene expression, migration and inflammation. Activation of Rho-GTPases has been linked to podocyte dysfunction, a feature of chronic kidney diseases (CKD). We investigated the effect of Rac-1 and Rho kinase (ROCK) inhibition on progressive renal failure in mice and studied the underlying mechanisms in podocytes. SV129 mice were subjected to 5/6-nephrectomy which resulted in arterial hypertension and albuminuria. Subgroups of animals were treated with the Rac-1 inhibitor EHT1846, the ROCK inhibitor SAR407899 and the ACE inhibitor Ramipril. Only Ramipril reduced hypertension. In contrast, all inhibitors markedly attenuated albumin excretion as well as glomerular and tubulo-interstitial damage. The combination of SAR407899 and Ramipril was more effective in preventing albuminuria than Ramipril alone. To study the involved mechanisms, podocytes were cultured from SV129 mice and exposed to static stretch in the Flexcell device. This activated RhoA and Rac-1 and led via TGFβ to apoptosis and a switch of the cells into a more mesenchymal phenotype, as evident from loss of WT-1 and nephrin and induction of α-SMA and fibronectin expression. Rac-1 and ROCK inhibition as well as blockade of TGFβ dramatically attenuated all these responses. This suggests that Rac-1 and RhoA are mediators of podocyte dysfunction in CKD. Inhibition of Rho-GTPases may be a novel approach for the treatment of CKD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.