1. Stanley Nattel JACEP 2017;3:425-435
Major Profibrotic Signaling Pathways Involved in Atrial Fibrosis Pathways are interlinked, and some produce positive feedback that is important in fibrosis. αβ = integrin receptor α and β subunits; AngII = angiotensin-II; AP = activator protein; AT1R = angiotensin type 1 receptor; CTGF = connective tissue growth factor; DAG = diacylglycerol; ER = endoplasmic reticulum; ERK1/2 = extracellular signal-related kinase–1/2; Grb2 = growth-factor receptor-binding protein 2; IP3 = inositol-1,4,5-trisphosphate; JAK = Janus kinase; JNK = c-Jun N-terminal kinase; MAPK = mitogen-activated protein kinase; MMP = matrix metalloproteinase; NADPH = nicotine adenine dinucleotide-phosphate; NF-κB = nuclear factor-kappa B; PKC = protein kinase C; PDGF = platelet-derived growth factor; PDGFR = platelet-derived growth factor receptor; PIP2 = phosphatidylinositol bisphosphate; PLC = phospholipase C; ROS = reactive oxygen species; Shc = src homologous and collagen protein; SMA = smooth muscle actin; SMAD = sma- and mad-related proteins; SOS = son of sevenless protein; Src = sarcoma proto-oncogene tyrosine kinase; STAT = signal transducers and activators of transcription; TAK1 = TGFβ1-activated kinase–1; TF = transcription factor; TGFβ = transforming growth factor beta; TGF-βR = transforming growth factor-beta receptor; TIMP = tissue inhibitor of matrix metalloproteinase; TSS = transcriptional start site.
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2017 American College of Cardiology Foundation