ArticleJournal of cellular and molecular medicine2020
Aldosterone enhances high phosphate-induced vascular calcification through inhibition of AMPK-mediated autophagy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Hyperaldosteronism in the Pathophysiology and Management of Cardiovascular-Kidney-Metabolic Syndrome.Diabetes, obesity & metabolism · 2026Review
- Mineralocorticoid Receptor Antagonists in Dialysis.American journal of nephrology · 2026Review
- Identification of Epigenetic Regulators of Vascular Calcification with a CRISPR-Based Screen.Journal of the American Society of Nephrology : JASN · 2025Article
- Aldosterone promotes calcification of vascular smooth muscle cells in mice through the AIF-1/Wnt/β-catenin signaling pathway.International urology and nephrology · 2025Article
- Review
- Mineralocorticoid Receptors in Vascular Smooth Muscle: Blood Pressure and Beyond.Hypertension (Dallas, Tex. : 1979) · 2024Review
- AMPK-mediated autophagy is involved in the protective effect of canagliflozin in the vitamin D3 plus nicotine calcification model in rats.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Review
- Cardiovascular Disease in Obstructive Sleep Apnea: Putative Contributions of Mineralocorticoid Receptors.International journal of molecular sciences · 2023Review
- Autophagy Is Required to Sustain Increased Intestinal Cell Proliferation during Phenotypic Plasticity Changes in Honey Bee (International journal of molecular sciences · 2023Article
- Antihypertensive treatment with hydrochlorothiazide-hydralazine combination aggravates medial vascular calcification in CKD rats with mineral bone disorder.Frontiers in cardiovascular medicine · 2023Article
- Effect of eplerenone on cognitive impairment in spontaneously hypertensive rats.American journal of translational research · 2022Article
- Deletion of soluble epoxide hydrolase suppressed chronic kidney disease-related vascular calcification by restoring Sirtuin 3 expression.Cell death & disease · 2021Article
- Roles of Nuclear Receptors in Vascular Calcification.International journal of molecular sciences · 2021Review
- Article
- AMPK: Potential Therapeutic Target for Vascular Calcification.Frontiers in cardiovascular medicine · 2021Review
- β-Hydroxybutyric Inhibits Vascular Calcification via Autophagy Enhancement in Models Induced by High Phosphate.Frontiers in cardiovascular medicine · 2021Article
- Aldosterone enhances high phosphate-induced vascular calcification through inhibition of AMPK-mediated autophagy.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It remains unclear whether the necessity of calcified mellitus induced by high inorganic phosphate (Pi) is required and the roles of autophagy plays in aldosterone (Aldo)-enhanced vascular calcification (VC) and vascular smooth muscle cell (VSMC) osteogenic differentiation. In the present study, we found that Aldo enhanced VC both in vivo and in vitro only in the presence of high Pi, alongside with increased expression of VSMC osteogenic proteins (BMP2, Runx2 and OCN) and decreased expression of VSMC contractile proteins (α-SMA, SM22α and smoothelin). However, these effects were blocked by mineralocorticoid receptor inhibitor, spironolactone. In addition, the stimulatory effects of Aldo on VSMC calcification were further accelerated by the autophagy inhibitor, 3-MA, and were counteracted by the autophagy inducer, rapamycin. Moreover, inhibiting adenosine monophosphate-activated protein kinase (AMPK) by Compound C attenuated Aldo/MR-enhanced VC. These results suggested that Aldo facilitates high Pi-induced VSMC osteogenic phenotypic switch and calcification through MR-mediated signalling pathways that involve AMPK-dependent autophagy, which provided new insights into Aldo excess-associated VC in various settings.
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