S100A8 and hydrops fetalis: CD11b+Gr1+ neutrophil-derived S100A8/A9 proteins participate in angiotensin II-induced cardiac inflammation and fibrosis, activating NF-κB signaling in cardiac fibroblasts via RAGE and amplifying chemokine and cytokine production, thus intensifying the inflammatory response and cardiac remodeling that characterize HF progression (27).