YEN-HUNG LINChou C.-H.Wu X.-M.Chang Y.-Y.CHI-SHENG HUNGYING-HSIEN CHENTzeng Y.-L.VIN-CENT WUYI-LWUN HOFON-JOU HSIEHKWAN-DUN WU2020-09-282020-09-2820141932-6203https://www.scopus.com/inward/record.uri?eid=2-s2.0-84907462313&doi=10.1371%2fjournal.pone.0095254&partnerID=40&md5=c1993140bfcc0f59437410da95436ca6https://scholars.lib.ntu.edu.tw/handle/123456789/515096https://pubmed.ncbi.nlm.nih.gov/25180794/Context: Patients with primary aldosteronism are associated with increased myocardial fibrosis. Galectin-3 is one of the most important mediators between macrophage activation and myocardial fibrosis. Objective: To investigate whether aldosterone induces galectin-3 secretion in vitro and in vivo. Methods and results: We investigated the possible molecular mechanism of aldosterone-induced galectin-3 secretion in macrophage cell lines (THP-1 and RAW 264.7 cells). Aldosterone induced galectin-3 secretion through mineralocorticoid receptors via the PI3K/Akt and NF-κB transcription signaling pathways. In addition, aldosterone-induced galectin-3 expression enhanced fibrosis-related factor expression in fibroblasts. We observed that galectin-3 mRNA from peripheral blood mononuclear cells and serum galectin-3 levels were both significantly increased in mice implanted with aldosterone pellets on days 7 and 14. We then conducted a prospective preliminary clinical study to investigate the association between aldosterone and galectin-3. Patients with aldosterone-producing adenoma had a significantly higher plasma galectin-3 level than patients with essential hypertension. One year after adrenalectomy, the plasma galectin-3 level had decreased significantly in the patients with aldosterone-producing adenoma. Conclusion: This study demonstrated that aldosterone could induce galectin-3 secretion in vitro and in vivo.journal article10.1371/journal.pone.0095254251807942-s2.0-84907462313