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. 2023 Feb 3;12(3):e028121. doi: 10.1161/JAHA.122.028121

Figure 3. Mechanotransduction of increased cyclic stretch because of left heart failure in endothelial cells, fibroblasts, and smooth muscle cells triggers a cascade of pathologic vascular remodeling.

Figure 3

Boxes within the cell signaling cascade are colored to match their corresponding box at the top of the figure (altered biomechanics, mechanotransduction, or vascular remodeling). AKT indicates protein kinase B; cAMP indicates cyclic adenosine monophosphate; Cox‐2 indicates cyclooxygenase‐2; ECM, extracellular matrix; eNOS, endothelial nitric oxide synthase; ERK, extracellular signal‐regulated kinase; FAK, focal adhesion kinase; FGF‐2, fibroblast growth factor‐2; GPCR, G protein‐coupled receptor; IGF‐1, insulin‐like growth factor‐1; IL‐6, interleukin‐6; JNK, c‐Jun N‐terminal kinase; MCP‐1, myocyte chemoattractant protein‐1; MMP, matrix metalloproteinase; NF‐κB, nuclear factor‐κB; NOX‐4, NADPH oxidase‐4; P13K, p13 kinase; PKA, protein kinase A; PKC, protein kinase C; PLC, phospholipase C; Rac1, Ras‐related C3 botulinum toxin substrate 1; RhoA, ras homolog family member A; ROS, reactive oxygen species; TGFβ, transforming growth factor beta; TNF‐α, tumor necrosis factor‐α; VCAM‐1, vascular cell adhesion protein 1; VE cadherin, vascular endothelial cadherin; and VEGF, vascular endothelial growth factor.