CTHRC1, or Collagen Triple Helix Repeat Containing 1, is a secreted glycoprotein. It plays a pivotal role in extracellular matrix (ECM) deposition and wound repair, and is a primary target of TGF-β signaling in fibrosis. CTHRC1 also modulates both the TGF-β and canonical Wnt signaling pathways, regulating tissue remodeling and homeostasis [1]. It is involved in various physiological processes such as metabolism, arterial remodeling, bone formation, and peripheral nervous system myelination [4].

In liver fibrosis, CTHRC1, derived from hepatic stellate cells (HSCs), promotes HSCs transformation to an activated state and enhances their migratory or contractile capacities by activating TGF-β signaling. CCl4 or TAA-induced liver fibrosis was attenuated in CTHRC1 -/- mice, and a monoclonal antibody of CTHRC1 suppressed liver fibrosis in wild-type mice, suggesting CTHRC1 as a regulator of liver fibrosis and a potential therapeutic target [2]. In the context of myocardial infarction, absence of CTHRC1 in mice led to pronounced lethality due to ventricular rupture, highlighting its role in the healing scar process [3]. Also, Cthrc1 deficiency in mice aggravated cardiac function, reduced collagen deposition, and increased mortality from cardiac rupture after myocardial infarction, and these effects could be partly reversed by rCTHRC1 or rWNT5A protein, indicating CTHRC1's role in wound repair and preventing cardiac rupture via the non-canonical WNT5A-PCP signaling pathway [5].

In conclusion, CTHRC1 is crucial for ECM deposition, wound repair, and tissue homeostasis. Studies using gene knockout mouse models have revealed its significant roles in fibrotic diseases such as liver fibrosis and in post-myocardial infarction wound repair. These findings suggest CTHRC1 as a potential biomarker and therapeutic target for related diseases.