File:Ijms-23-09243-g001-550.webp

English: Figure 1. Components of pathophysiological MR overactivation that are counteracted by finerenone in different organs and cell types, including relevant biomarkers. Antagonism by finerenone counteracts the pathophysiological components of MR overactivation including sodium retention, ROS generation and endothelial dysfunction, inflammation, fibrosis, ECM remodeling and hypertrophy. Biomarkers with a modified expression induced by MR antagonism with finerenone in diverse preclinical disease models are depicted around the mechanistic components. Organs including critical functional units (e.g., retina in the eye, alveolus in the lung, and glomerulus in the kidney) and relevant specific cell types (e.g., fibroblasts in light blue and macrophages in yellow) with a documented MR-based pathophysiology, as described in the text, are framing the view. αSMA, alpha smooth muscle actin; ADAMTS1, a disintegrin and metalloproteinase with thrombospondin type 1 motif 1; BNP, B-type natriuretic peptide; CD68, cluster of differentiation 68; CTGF, connective tissue growth factor; ECM, extracellular matrix; Gal-3, galectin-3; IL, interleukin; KIM-1, kidney injury molecule 1; LOX, lysyl oxidase; MCP-1, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; NGAL, neutrophil gelatinase-associated lipocalin; NKD2, naked cuticle homolog 2; OPN, osteopontin; PAI-1, plasminogen activator inhibitor-1; ROS, reactive oxygen species; Sgk1, serum- and glucocorticoid-regulated kinase 1; SOD, superoxide dismutase; TGF-β, transforming growth factor-β; TNF-α, tumor necrosis factor-α; Tnx, tenascin-X; UCP-1, uncoupling protein-1.