MALAT1: A novel hypothesis on the pathology of vascular injury in patients with β-thalassemia

Abstract

Vascular injury is a common consequence in β-thalassemia patients with severe anemia. Vascular cell damage can result in cardiomyopathy, thrombosis, and persistent ulceration. Although it has been suggested that injury is caused by iron accumulation and oxidative stress, the exact molecular mechanism remains unknown. Here, we highlight the potential role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in this pathophysiology. This hypothesis is based on the literature, which demonstrates that lncRNA expression of MALAT1-lncRNA is linked to vascular damage, wound healing capability, and cardiomyopathy. Furthermore, various technologies can be employed to manipulate the expression of MALAT1-lncRNA. In light of these studies, assessment of MALAT1 expression may enhance our understanding of the molecular pathophysiology of vascular damage in β-thalassemia. If confirmed, elevated MALAT1 expression could serve as a promising target for expediting the healing process in pathogenic tissues. Additionally, MALAT1 may serve as a surrogate biomarker for therapeutic management of patients with β-thalassemia who have vascular complications.