Adipokine Nesfatin-1 Mediates Endothelial Dysfunction by Suppressing MEF2B/ BMPR1A During Pulmonary Vascular Remodeling - PubMed
3 hours ago
- #Pulmonary Hypertension
- #Adipokines
- #Endothelial Dysfunction
- Perivascular adipose tissue (PVAT) dysfunction contributes to pulmonary vascular remodeling in pulmonary hypertension.
- Nesfatin-1, an adipokine from dysfunctional PVAT, is a key mediator in endothelial dysfunction and pulmonary vascular remodeling.
- Browning white adipose tissue with CL-316243 or deleting nesfatin-1 in lung adipocytes attenuates pulmonary hypertension in mouse models.
- IL-17/Th17 induces nesfatin-1 secretion via the PI3K/AKT/mTOR pathway.
- Nesfatin-1 promotes endothelial cell angiogenesis, adhesion, and apoptosis, and downregulates BMPR1A via MEF2B at transcriptional and posttranslational levels.
- Targeting PVAT and nesfatin-1 may offer new therapeutic strategies for pulmonary hypertension.