Actin alpha 2 (smooth muscle) (ACTA2)

Actin alpha 2 (ACTA2), also known as alpha-smooth muscle actin (α-SMA), is a highly conserved cytoskeletal protein that serves as a primary component of the contractile apparatus in smooth muscle cells. It plays a vital role in maintaining vascular tone and blood pressure homeostasis by interacting with myosin to generate mechanical tension within the arterial walls [2, 5, 10]. Beyond its structural function, ACTA2 is a critical biomarker for myofibroblast activation and epithelial-mesenchymal transition (EMT), making it a key indicator of tissue fibrosis and cancer progression in various organs [1, 3, 6]. Mutations in the ACTA2 gene are associated with life-threatening vascular conditions, including familial thoracic aortic aneurysms and dissections (TAAD), early-onset coronary artery disease, and multisystemic smooth muscle dysfunction syndrome (MSMDS) [5, 11, 16]. While current clinical management focuses on managing vascular symptoms using drugs like beta-blockers and ARBs, the protein is a significant target for anti-fibrotic drug development and experimental gene-editing therapies [14, 17]. Its essential role in global smooth muscle function presents a challenge for systemic targeting, often requiring localized or indirect modulation of its expression pathways [11, 19].

Other names

Alpha-smooth muscle actinα-SMAAlpha-actin-2Aortic smooth muscle actinACTSAAAT6MYMY5SMDYSGrowth-inhibiting gene 46

Modulation of vascular tone, inhibition of myofibroblast activation, regulation of TGF-beta signaling, and stabilization of actin filaments.