Key result
Endothelial dysfunction plays a key role in the initiation and progression of pulmonary hypertension, with new insights emerging from multi-omic studies and organ-on-chip technologies.
Why the study?
Recent genomic, transcriptomic, and metabolomic studies alongside novel organ-on-chip technologies have provided new insights into the role of endothelial dysfunction in the pathogenesis of pulmonary hypertension.
This review synthesizes recent multi-omic and organ-on-chip data to provide updated insights into the critical role of endothelial dysfunction in the pathogenesis of pulmonary hypertension.
Supports endothelial-targeted strategies in pulmonary hypertension; extends mechanistic understanding via multi-omic and organ-on-chip data but leaves clinical translation open.
Endothelial dysfunction plays a key role in the initiation and progression of pulmonary hypertension (PH), a fatal and currently incurable disease associated with increased pulmonary vascular resistance and leading to right heart failure. Recent data from genomic, transcriptomic and metabolomic studies and emergence of novel organ-on-chip technologies have provided new insights into the role of endothelium in the pathogenesis of this disease. In this review, we characterise key features of endothelial dysfunction in PH, highlighting the diversity of endothelial cell types and differences in their responses to vascular insults. We also present the current understanding of the effects of genetic mutations on endothelial function and comment on new ways of disease modelling using organ-on-chip technologies.
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Haensel et al. (2023) conducted a review in Pulmonary hypertension. Endothelial dysfunction was evaluated. Endothelial dysfunction plays a key role in the initiation and progression of pulmonary hypertension, with new insights emerging from multi-omic studies and organ-on-chip technologies.
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