Trans-2,3-enoyl-CoA reductase-like protein (TECRL)

Trans-2,3-enoyl-CoA reductase-like protein (TECRL) is an endoplasmic reticulum-resident enzyme with oxidoreductase activity, predominantly expressed in cardiac and skeletal muscle[1][2][3]. TECRL is structurally related to steroid 5-alpha-reductases and has domains associated with fatty acid metabolism, including a ubiquitin-like domain at the N-terminus and a 3-oxo-5-alpha steroid 4-dehydrogenase domain at the C-terminus[2][3]. Functionally, it is implicated in the biosynthesis of very long-chain fatty acids, regulation of mitochondrial integrity, muscle regeneration via satellite cell activation, and control of the cell cycle in myoblasts through ERK1/2 and EGR2 signaling pathways[1][3]. Pathogenic mutations in TECRL are causatively linked to catecholaminergic polymorphic ventricular tachycardia type 3 (CPVT3) and long QT syndrome, reflecting its critical role in cardiac excitability and conduction[4]. There are no currently approved drugs that specifically target TECRL, but it is emerging as a potential therapeutic target in regenerative muscle medicine and cardiology.

Other names

TECRLSRD5A2L2GPSN2LTERLCPVT3Steroid 5-alpha-reductase 2-like 2 proteinGlycoprotein, synaptic 2-liketrans-2,3-enoyl-CoA reductase-like

No approved drugs directly target TECRL; mechanism may involve modulation of mitochondrial or fatty acid metabolism pathways[2][3][4].