MALAT1: A novel hypothesis on the pathology of vascular injury in patients with β-thalassemia
Issued Date
2024-01-01
Resource Type
ISSN
03069877
eISSN
15322777
Scopus ID
2-s2.0-85180424515
Journal Title
Medical Hypotheses
Volume
182
Rights Holder(s)
SCOPUS
Bibliographic Citation
Medical Hypotheses Vol.182 (2024)
Suggested Citation
Noulsri E., Lerdwana S. MALAT1: A novel hypothesis on the pathology of vascular injury in patients with β-thalassemia. Medical Hypotheses Vol.182 (2024). doi:10.1016/j.mehy.2023.111232 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/95557
Title
MALAT1: A novel hypothesis on the pathology of vascular injury in patients with β-thalassemia
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Author's Affiliation
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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.