Buonafine, MathieuMartínez Martínez, ErnestoJaisser, Frédéric2026-02-092026-02-092018-02-06Buonafine M, Martínez-Martínez E, Amador C, Gravez B, Ibarrola J, Fernández-Celis A, El Moghrabi S, Rossignol P, López-Andrés N, Jaisser F. Neutrophil Gelatinase-Associated Lipocalin from immune cells is mandatory for aldosterone-induced cardiac remodeling and inflammation. J Mol Cell Cardiol. 2018 Feb;115:32-38.0022-282810.1016/j.yjmcc.2017.12.011https://hdl.handle.net/20.500.14352/131855Immune system activation is involved in cardiovascular (CV) inflammation and fibrosis, following activation of the mineralocorticoid receptor (MR). We previously showed that Neutrophil Gelatinase-Associated Lipocalin (NGAL) is a novel target of MR signaling in CV tissue and plays a critical role in aldosterone/MR-dependent hypertension and fibrosis. We hypothesized that the production of NGAL by immune cells may play an important part in the mediation of these deleterious mineralocorticoid-induced effects. We analyzed the effect of aldosterone on immune cell recruitment and NGAL expression in vivo. We then studied the role of NGAL produced by immune cells in aldosterone-mediated cardiac inflammation and remodeling using mice depleted for NGAL in their immune cells by bone marrow transplantation and subjected to mineralocorticoid challenge NAS (Nephrectomy, Aldosterone 200μg/kg/day, Salt 1%). NAS treatment induced the recruitment of various immune cell populations to lymph nodes (granulocytes, B lymphocytes, activated CD8+ T lymphocytes) and the induction of NGAL expression in macrophages, dendritic cells, and PBMCs. Mice depleted for NGAL in their immune cells were protected against NAS-induced cardiac remodeling and inflammation. We conclude that NGAL produced by immune cells plays a pivotal role in cardiac damage under mineralocorticoid excess. Our data further stressed a pathogenic role of NGAL in cardiac damages, besides its relevance as a biomarker of renal injury.engjournal article1095-8584https://doi.org/10.1016/j.yjmcc.2017.12.01129289651https://www.sciencedirect.com/science/article/pii/S002228281730367Xhttps://pubmed.ncbi.nlm.nih.gov/29289651/restricted access616.12AldosteroneCardiovascularFibrosisInflammationMRNGALCardiología3207.04 Patología Cardiovascular