ArticleMolecular and cellular endocrinology2016
VLDL-activated cell signaling pathways that stimulate adrenal cell aldosterone production.
Article in Molecular and cellular endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Very low-density lipoprotein and the human health.World journal of experimental medicine · 2026Review
- Lipid metabolism in the adrenal gland.Frontiers in endocrinology · 2025Review
- Discovery of RXFP2 genetic association in resistant hypertensive men and RXFP2 antagonists for the treatment of resistant hypertension.Scientific reports · 2024Article
- Emerging Evidence of Pathological Roles of Very-Low-Density Lipoprotein (VLDL).International journal of molecular sciences · 2022Review
- The role of lipid second messengers in aldosterone synthesis and secretion.Journal of lipid research · 2022Review
- The fatty acid elongase ELOVL6 regulates bortezomib resistance in multiple myeloma.Blood advances · 2021Article
- Lipid profile and left ventricular geometry pattern in obese children.Lipids in health and disease · 2020Article
- Lipoproteins modulate growth and P-glycoprotein expression in drug-resistant HER2-overexpressed breast cancer cells.Heliyon · 2019Article
- Aging and Adrenal Aldosterone Production.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Very low-density lipoprotein (VLDL)-induced signals mediating aldosterone production.The Journal of endocrinology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Aldosterone plays an important role in regulating ion and fluid homeostasis and thus blood pressure, and hyperaldosteronism results in hypertension. Hypertension is also observed with obesity, which is associated with additional health risks, including cardiovascular disease. Obese individuals have high serum levels of very low-density lipoprotein (VLDL), which has been shown to stimulate aldosterone production; however, the mechanisms underlying VLDL-induced aldosterone production are still unclear. Here we demonstrate in human adrenocortical carcinoma (HAC15) cells that submaximal concentrations of angiotensin II and VLDL stimulate aldosterone production in an additive fashion, suggesting the possibility of common mechanisms of action. We show using inhibitors that VLDL-induced aldosterone production is mediated by the PLC/IP3/PKC signaling pathway. Our results suggest that PKC is upstream of the extracellular signal-regulated kinase (ERK) activation previously observed with VLDL. An understanding of the mechanisms mediating VLDL-induced aldosterone production may provide insights into therapies to treat obesity-associated hypertension.
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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 Socratic graph.