Skip to main content
. 2025 Sep 23;12:1506190. doi: 10.3389/fcvm.2025.1506190

Figure 1.

Diagram illustrating signaling pathways affecting cardiac function. Ang2 activates ATR1, leading to ENAC and NHE3 activation, consuming ATP, and aggravating cardiac impairment via AQP2 increase. A stimulatory ligand activates adenyl cyclase (AC) via a G protein, converting ATP to cAMP, activating protein kinase A, resulting in a cellular response. An inhibitory ligand reduces AC activity. Pro ANP improves cardiac function by affecting AQP2.

Mechanisms by which traditional Chinese medicine regulates AQP2 in water metabolism disorders. AQP2-mediated regulation of renal water balance is intimately linked to the development and progression of heart failure. Angiotensin II (Ang II) engages AT1 receptors to trigger the ENaC/NHE3 pathway, leading to VP release and increased aldosterone production. These hormonal signals synergistically elevate AQP2 expression in renal collecting duct cells, resulting in fluid retention and hyponatremia that worsen heart failure symptoms. In contrast, the serine protease Corin converts pro-ANP into its active form, ANP, which suppresses AQP2 expression, and ultimately improving the clinical manifestations of heart failure.