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< em > SOX17 < /em > Enhancer Variants Disrupt Transcription Factor Binding And Enhancer Inactivity Drives Pulmonary Hypertension
CONCLUSIONS: Common PAH risk variants upstream of the SOX17 promoter reduce endothelial SOX17 expression, at least in part, through differential binding of HOXA5 and ROR-α. Reduced SOX17 expression results in disturbed hPAEC function and PAH. Existing drug compounds can reverse the disturbed SOX17 pulmonary endothelial transcriptomic signature.PMID:37066790 | DOI:10.1161/CIRCULATIONAHA.122.061940
Source: Circulation - April 17, 2023 Category: Cardiology Authors: Rachel Walters Eleni Vasilaki Jurjan Aman Chien-Nien Chen Yukyee Wu Olin D Liang Ali Ashek Olivier Dubois Lin Zhao Farah Sabrin In ês Cebola Jorge Ferrer Nicholas W Morrell James R Klinger Martin R Wilkins Lan Zhao Christopher J Rhodes Source Type: research

Endothelial Foxp1 Regulates Pathological Cardiac Remodeling Through TGF- β1-Endothelin-1 Signal Pathway.
CONCLUSIONS: EC-Foxp1 regulates the TGF-β1-ET-1 pathway to control pathological cardiac fibrosis and hypertrophy, resulting in cardiac dysfunction. Therefore, targeting the EC-Foxp1-TGF-β1-ET-1 pathway might provide a future novel therapy for heart failure. PMID: 31177814 [PubMed - as supplied by publisher]
Source: Circulation - June 9, 2019 Category: Cardiology Authors: Liu J, Zhuang T, Pi J, Chen X, Zhang Q, Li Y, Wang H, Shen Y, Tomlinson B, Chan P, Yu Z, Cheng Y, Zheng X, Reilly M, Morrisey E, Zhang L, Liu Z, Zhang Y Tags: Circulation Source Type: research

The Long Non-Coding RNA CPR Regulates Cardiomyocyte Proliferation and Cardiac Repair.
CONCLUSIONS: Together, our findings identified that CPR is a suppressor of cardiomyocyte proliferation, and it indicates that lncRNA(s) take parts in the regulation of cardiomyocyte proliferation and cardiac repair. Our study provides an lncRNA-based therapeutic strategy for effective cardiac repair and regeneration. PMID: 30832495 [PubMed - as supplied by publisher]
Source: Circulation - March 4, 2019 Category: Cardiology Authors: Ponnusamy M, Liu F, Zhang YH, Li RB, Zhai M, Liu F, Zhou LY, Liu CY, Yan KW, Dong YH, Wang M, Qian LL, Shan C, Xu S, Wang Q, Zhang YH, Li PF, Zhang J, Wang K Tags: Circulation Source Type: research

Rearrangement of the Protein Phosphatase 1 Interactome During Heart Failure Progression.
Conclusions -PP1 is best studied at the level of its interactome, which undergoes significant rearrangement during HF progression. The nine key interactors that are associated with HF progression may represent potential targets in HF therapy. In particular, Ppp1r7 may play a central role in regulating the PP1 interactome by acting as a competitive molecular "sponge" of PP1c. PMID: 29669786 [PubMed - as supplied by publisher]
Source: Circulation - April 18, 2018 Category: Cardiology Authors: Chiang DY, Alsina KM, Corradini E, Fitzpatrick M, Ni L, Lahiri SK, Reynolds J, Pan X, Scott L, Heck AJR, Wehrens XH Tags: Circulation Source Type: research

Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure.
Conclusions -Our results identify a novel functional role for BMP9 as an endogenous inhibitor of cardiac fibrosis due to LV pressure overload and further show that treatment with either recombinant BMP9 or disruption of endoglin activity promotes BMP9 activity and limits cardiac fibrosis in heart failure, thereby providing potentially novel therapeutic approaches for patients with heart failure. PMID: 29487140 [PubMed - as supplied by publisher]
Source: Circulation - February 27, 2018 Category: Cardiology Authors: Morine KJ, Qiao X, York S, Natov PS, Paruchuri V, Zhang Y, Aronovitz MJ, Karas RH, Kapur NK Tags: Circulation Source Type: research

miR-195 Regulates Metabolism in Failing Myocardium via Alterations in SIRT3 Expression and Mitochondrial Protein Acetylation.
Conclusions -Altogether, these data suggest that increased levels of miR-195 in failing myocardium regulate a novel pathway that involves direct SIRT3 suppression and enzymatic inhibition via increased acetylation of PDH and ATP synthase that are essential for cardiac energy metabolism. PMID: 29330215 [PubMed - as supplied by publisher]
Source: Circulation - January 12, 2018 Category: Cardiology Authors: Zhang X, Ji R, Liao X, Castillero E, Kennel PJ, Brunjes DL, Franz M, Möbius-Winkler S, Drosatos K, George I, Chen EI, Colombo PC, Schulze PC Tags: Circulation Source Type: research