Journal
CARDIOVASCULAR RESEARCH
Volume 116, Issue 12, Pages 1937-1947Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvaa050
Keywords
PAH; Pathogenesis; lncRNA; Smooth muscle cell dysregulation; Endothelial dysfunction; EndMT
Categories
Funding
- National Natural Science Foundation of China [81570046, 81700054, 81870045, 81970053, 81970054, 91739109]
- Guangdong Provincial Key Laboratory of Regional Immunity and Diseases [2019B030301009]
- Interdisciplinary Innovation Team Project of Shenzhen University
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Pulmonary arterial hypertension (PAH) is a disease with complex pathobiology, significant morbidity and mortality, and remains without a cure. It is characterized by vascular remodelling associated with uncontrolled proliferation of pulmonary artery smooth muscle cells, endothelial cell proliferation and dysfunction, and endothelial-tomesenchymal transition, leading to narrowing of the vascular Lumen, increased vascular resistance and pulmonary arterial pressure, which inevitably results in right heart failure and death. There are multiple molecules and signalling pathways that are involved in the vascular remodelling, including non-coding RNAs, i.e. microRNAs and long noncoding RNAs (lncRNAs). It is only in recent years that the role of lncRNAs in the pathobiology of pulmonary vascular remodelling and right ventricular dysfunction is being vigorously investigated. In this review, we have summarized the current state of knowledge about the role of lncRNAs as key drivers and gatekeepers in regulating major cellular and molecular trafficking involved in the pathogenesis of PAH. In addition, we have discussed the limitations and challenges in translating lncRNA research in vivo and in therapeutic applications of lncRNAs in PAH.
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