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1. High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.

2. Reduced FOXF1 links unrepaired DNA damage to pulmonary arterial hypertension.

3. Dysregulated Smooth Muscle Cell BMPR2-ARRB2 Axis Causes Pulmonary Hypertension.

4. Endogenous Retroviral Elements Generate Pathologic Neutrophils in Pulmonary Arterial Hypertension.

5. KLF4 recruits SWI/SNF to increase chromatin accessibility and reprogram the endothelial enhancer landscape under laminar shear stress.

6. Monocyte-released HERV-K dUTPase engages TLR4 and MCAM causing endothelial mesenchymal transition.

7. ALDH1A3 Coordinates Metabolism With Gene Regulation in Pulmonary Arterial Hypertension.

8. PPARγ-p53-Mediated Vasculoregenerative Program to Reverse Pulmonary Hypertension.

9. Intrinsic Endocardial Defects Contribute to Hypoplastic Left Heart Syndrome.

10. Cellular senescence impairs the reversibility of pulmonary arterial hypertension.

11. Clinical trial in a dish using iPSCs shows lovastatin improves endothelial dysfunction and cellular cross-talk in LMNA cardiomyopathy.

12. In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug.

13. FGF2 inhibits endothelial-mesenchymal transition through microRNA-20a-mediated repression of canonical TGF-β signaling.

14. Endothelial Plasticity: Shifting Phenotypes through Force Feedback.

15. Endothelial-to-mesenchymal transition contributes to fibro-proliferative vascular disease and is modulated by fluid shear stress.

16. Erk5 inhibits endothelial migration via KLF2-dependent down-regulation of PAK1.

17. The flow dependency of Tie2 expression in endotoxemia.

18. IL-1β and TGFβ2 synergistically induce endothelial to mesenchymal transition in an NFκB-dependent manner.

19. Cellular plasticity: the good, the bad, and the ugly? Microenvironmental influences on progenitor cell therapy.

20. Endothelial progenitor cells give rise to pro-angiogenic smooth muscle-like progeny.

21. Pleiotropism of adiponectin: inflammation, neovascularization, and fibrosis.

22. Generating new blood flow: integrating developmental biology and tissue engineering.

23. Reduced number and impaired function of circulating progenitor cells in patients with systemic lupus erythematosus.

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