ArticleExperimental cell research2012
Shear stress induces cell apoptosis via a c-Src-phospholipase D-mTOR signaling pathway in cultured podocytes.
Article in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 58 citations in OpenAlex.
- Protection against cisplatin-induced acute kidney injury by hellgrammite extract: insights from comprehensive metabolomics.Frontiers in pharmacology · 2026Article
- Obesity-Related Glomerulosclerosis-How Adiposity Damages the Kidneys.International journal of molecular sciences · 2025Review
- mTORC1 signaling and diabetic kidney disease.Diabetology international · 2024Review
- ScRNA-seq revealed the tumor microenvironment heterogeneity related to the occurrence and metastasis in upper urinary tract urothelial carcinoma.Cancer gene therapy · 2024Article
- ScRNA-seq revealed an immunosuppression state and tumor microenvironment heterogeneity related to lymph node metastasis in prostate cancer.Experimental hematology & oncology · 2023Article
- Kidney-on-a-Chip: Mechanical Stimulation and Sensor Integration.Sensors (Basel, Switzerland) · 2022Review
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- Glomerular Biomechanical Stress and Lipid Mediators during Cellular Changes Leading to Chronic Kidney Disease.Biomedicines · 2022Review
- Antiproteinuric and Hyperkalemic Mechanisms Activated by Dual Versus Single Blockade of the RAS in Renovascular Hypertensive Rats.Frontiers in physiology · 2021Article
- Upregulated proteoglycan-related signaling pathways in fluid flow shear stress-treated podocytes.American journal of physiology. Renal physiology · 2020Article
- Fyn Kinase: A Potential Therapeutic Target in Acute Kidney Injury.Biomolecules & therapeutics · 2020Review
- Mechanisms of Synergistic Interactions of Diabetes and Hypertension in Chronic Kidney Disease: Role of Mitochondrial Dysfunction and ER Stress.Current hypertension reports · 2020Review
- Hyperfiltration-mediated Injury in the Remaining Kidney of a Transplant Donor.Transplantation · 2018Review
- Phospholipase D1 regulation of TNF-alpha protects against responses to LPS.Scientific reports · 2018Article
- Mechanotransduction signaling in podocytes from fluid flow shear stress.American journal of physiology. Renal physiology · 2018Article
- Src family kinases in chronic kidney disease.American journal of physiology. Renal physiology · 2017Review
- Stressed podocytes-mechanical forces, sensors, signaling and response.Pflugers Archiv : European journal of physiology · 2017Review
- Role of biomechanical forces in hyperfiltration-mediated glomerular injury in congenital anomalies of the kidney and urinary tract.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Review
- Development of a Functional Glomerulus at the Organ Level on a Chip to Mimic Hypertensive Nephropathy.Scientific reports · 2016Article
- Ivabradine Prevents Low Shear Stress Induced Endothelial Inflammation and Oxidative Stress via mTOR/eNOS Pathway.PloS one · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The glomerular capillary wall, composed of endothelial cells, the glomerular basement membrane and the podocytes, is continually subjected to hemodynamic force arising from tractional stress due to blood pressure and shear stress due to blood flow. Exposure of glomeruli to abnormal hemodynamic force such as hyperfiltration is associated with glomerular injury and progressive renal disease, and the conversion of mechanical stimuli to chemical signals in the regulation of the process is poorly understood in podocytes. By examining DNA fragmentation, apoptotic nuclear changes and cytochrome c release, we found that shear stress induced cell apoptosis in cultured podocytes. Meanwhile, podocytes exposed to shear stress also stimulated c-Src phosphorylation, phospholipase D (PLD) activation and mammalian target of rapamycin (mTOR) signaling. Using the antibodies against c-Src, PLD(1), and PLD(2) to perform reciprocal co-immunoprecipitations and in vitro PLD activity assay, our data indicated that c-Src interacted with and activated PLD(1) but not PLD(2). The inhibition of shear stress-induced c-Src phosphorylation by PP(2) (a specific inhibitor of c-Src kinase) resulted in reduced PLD activity. Phosphatidic acid, produced by shear stress-induced PLD activation, stimulated mTOR signaling, and caused podocyte hypertrophy and apoptosis.
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Registered trials
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.