Advance in Molecular Pathology of Pulmonary Hypertension
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (20 June 2023) | Viewed by 2512
Special Issue Editor
Interests: pulmonary hypertension; vasculature; endothelial cells; smooth muscle cells; mechanism of neointima formation; congenital heart defect
Special Issue Information
Dear Colleagues,
Pulmonary hypertension (PH) is a serious sequele of several systemic and genetic diseases, lung developmental and heart defects, and drug toxicity. A mean pulmonary artery pressure of >20 mmHg is diagnostic of PH. PH is associated with inflammation, altered vascular relaxation responses, cellular phenotype changes, and cell proliferation and migration, resulting in vascular remodeling and obstruction leading to PH, right ventricular hypertrophy, neointima formation, and metabolic alteration, which eventually result in heart failure and premature death. The sustained cell proliferation and apoptosis resistance, abnormal angiogenesis, and dysregulated cellular metabolism observed in PH are reminiscent of cancer. The molecular mechanism/s involved in the development and progression of PH is not yet fully understood. However, recent advances in the field have described several important aspects such as the deregulation of multiple genes and protein expressions, mitochondrial dysfunction, altered molecular pathways, autophagic dysregulation in pulmonary endothelial and smooth muscle cells, and the endothelial–mesenchymal transition in PH. Mitochondrial dysfunction is thought to contribute to the metabolic alterations observed in PH. These responses promote the survival of proliferating cells. A number of these molecules function as a double-edged sword. They maintain homeostasis under normal conditions but facilitate cell proliferation and migration in the disease state.
Dr. Rajamma Mathew
Guest Editor
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Keywords
- angiogenesis
- autophagy
- cell proliferation and migartion
- cell survival
- endothelial mesenchymal transition
- inflammation
- metabolic deregulation
- oxidant injury and stress
- pulmonary hypertension
