ArticleExperimental and molecular pathology2017
Vitamin D receptor deficit induces activation of renin angiotensin system via SIRT1 modulation in podocytes.
Article in Experimental and molecular pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association of vitamin D receptor TaqI and ApaI genetic polymorphisms with nephrolithiasis and end stage renal disease: a meta-analysis.BMC medical genetics · 2019Pooled it
- Vitamin D in Cardiovascular Medicine: From Molecular Mechanisms to Clinical Translation.Nutrients · 2026Review
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- APOL1 Dynamics in Diabetic Kidney Disease and Hypertension.Biomolecules · 2025Review
- The immunomodulatory potential of vitamin D on Th17 lymphocytes in systemic lupus erythematosus - a literature review.Medicine and pharmacy reports · 2025Review
- Correlation between orthostatic intolerance in children and levels of ACE2-Ang(1-7)-Mas axis and vitamin D.Frontiers in pediatrics · 2025Article
- APOL1 Modulates Renin-Angiotensin System.Biomolecules · 2024Article
- Physiological Evidence and Therapeutic Outcomes of Vitamin D on Cardiovascular Diseases.Current cardiology reviews · 2024Review
- A Quest for Potential Role of Vitamin D in Type II Diabetes Mellitus Induced Diabetic Kidney Disease.Current pharmaceutical design · 2024Review
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Secreted Cytokines within the Urine of AKI Patients Modulate TP53 and SIRT1 Levels in a Human Podocyte Cell Model.International journal of molecular sciences · 2023Article
- Vitamin D, Cellular Senescence and Chronic Kidney Diseases: What Is Missing in the Equation?Nutrients · 2023Review
- Article
- DNA methyltransferase 1 knockdown reverses PTEN and VDR by mediating demethylation of promoter and protects against renal injuries in hepatitis B virus-associated glomerulonephritis.Cell & bioscience · 2022Article
- The effects of exercise on kidney injury: the role of SIRT1.Molecular biology reports · 2022Review
- Potential Genes Associated with COVID-19 and Comorbidity.International journal of medical sciences · 2022Article
- Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70.Cells · 2021Review
- Vitamin D/VDR regulates peripheral energy homeostasis via central renin-angiotensin system.Journal of advanced research · 2021Article
- Nuclear receptors in podocyte biology and glomerular disease.Nature reviews. Nephrology · 2021Review
- Interplay between oxidative stress, SIRT1, reproductive and metabolic functions.Current research in physiology · 2021Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Vitamin D receptor (VDR) deficient status has been shown to be associated with the activation of renin angiotensin system (RAS). We hypothesized that lack of VDR would enhance p53 expression in podocytes through down regulation of SIRT1; the former would enhance the transcription of angiotensinogen (Agt) and angiotensinogen II type 1 receptor (AT1R) leading to the activation of RAS. Renal tissues of VDR mutant (M) mice displayed increased expression of p53, Agt, renin, and AT1R. In vitro studies, VDR knockout podocytes not only displayed up regulation p53 but also displayed enhanced expression of Agt, renin and AT1R. VDR deficient podocytes also displayed an increase in mRNA expression for p53, Agt, renin, and AT1R. Interestingly, renal tissues of VDR-M as well as VDR heterozygous (h) mice displayed attenuated expression of deacetylase SIRT1. Renal tissues of VDR-M mice showed acetylation of p53 at lysine (K) 382 residues inferring that enhanced p53 expression in renal tissues could be the result of ongoing acetylation, a consequence of SIRT1 deficient state. Notably, podocytes lacking SIRT1 not only showed acetylation of p53 at lysine (K) 382 residues but also displayed enhanced p53 expression. Either silencing of SIRT1/VDR or treatment with high glucose enhanced podocyte PPAR-y expression, whereas, immunoprecipitation (IP) of their lysates with anti-retinoid X receptor (RXR) antibody revealed presence of PPAR-y. It appears that either the deficit of SIRT1 has de-repressed expression of PPAR-y or enhanced podocyte expression of PPAR-y (in the absence of VDR) has contributed to the down regulation of SIRT1.
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