ArticleJournal of pharmacological sciences2013
Roles of Na⁺/H⁺ exchanger type 1 and intracellular pH in angiotensin II-induced reactive oxygen species generation and podocyte apoptosis.
Article in Journal of pharmacological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Autophagy and Mitophagy in Hypertensive Chronic Kidney Disease: Evidence Grading, Cell-Type Divergence, and a Working Lysosomal Hypothesis.Life (Basel, Switzerland) · 2026Review
- A Novel Role of Neutrophil Elastase in Podocyte Dysfunction Induced by High Glucose, PMA, and MDP.Journal of cellular physiology · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- The intelligent podocyte: sensing and responding to a complex microenvironment.Nature reviews. Nephrology · 2025Review
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Comparison between outcomes of IgA nephropathy with nephrotic-range proteinuria and nephrotic syndrome: do podocytes play a role?Renal failure · 2022Article
- Mitochondrial Oxidative Stress and Cell Death in Podocytopathies.Biomolecules · 2022Review
- Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022Review
- The role of extracellular vesicles in podocyte autophagy in kidney disease.Journal of cell communication and signaling · 2021Review
- Effects of the NaJournal of the renin-angiotensin-aldosterone system : JRAAS · 2021Review
- Research Progress on the Pathological Mechanisms of Podocytes in Diabetic Nephropathy.Journal of diabetes research · 2020Review
- Urinary levels of podocyte-derived microparticles are associated with the progression of chronic kidney disease.Annals of translational medicine · 2019Article
- Role of Podocyte Injury in Glomerulosclerosis.Advances in experimental medicine and biology · 2019Review
- Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-δ/p38 MAPK pathway activation and trough increased NaBMC nephrology · 2018Article
- PLK2 Plays an Essential Role in High D-Glucose-Induced Apoptosis, ROS Generation and Inflammation in Podocytes.Scientific reports · 2017Article
- Autophagy protects ovarian cancer-associated fibroblasts against oxidative stress.Cell cycle (Georgetown, Tex.) · 2016Article
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9 authors at 1 institution in 1 country.
Funding
Abstract
A growing body of evidence suggests that podocyte apoptosis is a major cause of decreased podocyte number, which leads to albuminuria and glomerular injury. The aim of this study was to clarify the molecular mechanisms of angiotensin II (Ang II)-induced apoptosis in cultured mouse podocytes. We examined the effects of Ang II (100 nmol/L) on apoptosis, superoxide anions, and cytosol pH in podocytes. For intracellular pH measurements, image analysis was conducted using confocal laser microscopy after incubation with carboxy-seminaphthorhodafluor-1. Superoxide anions and intracellular pH were elevated with Ang II treatment. Apoptotic cell numbers, as measured by TUNEL staining and caspase 3 activity, were also augmented in the Ang II-treated group. Pre-treatment with olmesartan (100 nmol/L, an Ang II type 1-receptor blocker), apocynin (50 μmol/L, NADPH oxidase inhibitor), or 5-N,N hexamethylene amiloride [30 μmol/L, Na⁺/H⁺ exchanger type 1 (NHE-1) inhibitor] abolished Ang II-induced podocyte apoptosis, whereas NHE-1 mRNA and protein expression was not affected by Ang II treatment. Moreover, Ang II increased NHE-1 phosphorylation. These results suggest that superoxide production, NHE-1 activation, and intracellular alkalization were early features prior to apoptosis in Ang II-treated mouse podocytes, and may offer new insights into the mechanisms responsible for Ang II-induced podocyte injury.
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