Journal
TRENDS IN MOLECULAR MEDICINE
Volume 27, Issue 3, Pages 280-292Publisher
CELL PRESS
DOI: 10.1016/j.molmed.2020.10.003
Keywords
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Funding
- National Institutes of Health [P50 DK-096373, R01 DK-116718, DK-116196, DK-096373, HL-148044]
- American Heart Association [18PRE34020090]
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The article discusses the origin, distribution, function, and plasticity of renin cells within the kidney and immune compartments, as well as the consequences of distorting the renin program. Understanding how chronic stimulation of these cells in the context of hypertension may lead to vascular pathology will serve as a foundation for targeted molecular therapies.
Hypotension and changes in fluid-electrolyte balance pose immediate threats to survival. Juxtaglomerular cells respond to such threats by increasing the synthesis and secretion of renin. In addition, smooth muscle cells (SMCs) along the renal arterioles transform into renin cells until homeostasis has been regained. However, chronic unrelenting stimulation of renin cells leads to severe kidney damage. Here, we discuss the origin, distribution, function, and plasticity of renin cells within the kidney and immune compartments and the consequences of distorting the renin program. Understanding how chronic stimulation of these cells in the context of hypertension may lead to vascular pathology will serve as a foundation for targeted molecular therapies.
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