Aldosterone synthesis and secretion
Core of basic research: Deciphers the regulatory mechanism of aldosterone synthesis and secretion by zona glomerulosa cells of the adrenal cortex, a key pathway maintaining water-sodium balance, blood pressure homeostasis, and electrolyte metabolism. The core regulatory axis is the renin-angiotensin-aldosterone system (RAAS): Angiotensin II (Ang II) binds to AT1R on zona glomerulosa cells, activating the PLC-γ-PKC pathway to promote the expression of CYP11B2 (aldosterone synthase), a key enzyme for aldosterone synthesis. Additionally, elevated blood potassium directly stimulates zona glomerulosa cells, activating calcium signaling via the calcium-sensing receptor (CaSR) to synergistically promote aldosterone secretion. Aldosterone acts on epithelial cells of the renal distal convoluted tubule and collecting duct, binding to the mineralocorticoid receptor (MR) to regulate the expression of ENaC and Na+/K+-ATPase, enhancing sodium reabsorption and potassium excretion. Research focuses on the specific regulation of Ang II-AT1R signaling, the synergistic secretion mechanism of blood potassium and Ang II, and pathway overactivation associated with primary aldosteronism, hypertension, and heart failure.
Core key proteins: Aldosterone, Angiotensin II (Ang II), AT1R (Ang II receptor), CYP11B2 (aldosterone synthase), CYP11B1 (11β-hydroxylase), PLC-γ, PKC, CaSR (calcium-sensing receptor), MR (mineralocorticoid receptor), ENaC (epithelial sodium channel), Na+/K+-ATPase, adrenal cortex zona glomerulosa cells, renal distal convoluted tubule epithelial cells.
Core key proteins: Aldosterone, Angiotensin II (Ang II), AT1R (Ang II receptor), CYP11B2 (aldosterone synthase), CYP11B1 (11β-hydroxylase), PLC-γ, PKC, CaSR (calcium-sensing receptor), MR (mineralocorticoid receptor), ENaC (epithelial sodium channel), Na+/K+-ATPase, adrenal cortex zona glomerulosa cells, renal distal convoluted tubule epithelial cells.
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