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. Author manuscript; available in PMC: 2024 May 6.
Published in final edited form as: J Med Chem. 2023 Aug 16;66(16):11027–11039. doi: 10.1021/acs.jmedchem.3c01178

Figure 3.

Figure 3.

(A) 5-HT2B-mediated recruitment of proangiogenic cells in pulmonary arterial hypertension leads to muscularization of pulmonary arterioles, shown by proliferation of pulmonary artery smooth muscle cells (PASMCs). (B) Valve remodeling in calcific aortic valve disease is driven by aortic valve interstitial cells (AVICs) that increase deposition of collagen and glycosaminoglycans (GAG) into the ECM; this stiffens the aortic valve leaflets and decreases valve compliance. It is unknown whether proangiogenic cells play a role in remodeling the valve ECM. (C) Myofibroblasts are responsible for ECM stiffening and scar tissue formation of the infarct zone in myocardial infarction, causing cardiac tissue deterioration, decreased compliance, and decreased cardiac output. Retrieved from https://app.biorender.com