Filtered By:
Specialty: Cardiology
Condition: Heart Failure

This page shows you your search results in order of date.

Order by Relevance | Date

Total 71 results found since Jan 2013.

< 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

Recombinant Adenovirus siRNA Knocking Down the Ndufs4 Gene Alleviates Myocardial Apoptosis Induced by Oxidative Stress Injury
In conclusion, we successfully constructed Ndufs4 siRNA recombinant adenovirus; furthermore, the downexpression of the Ndufs4 gene may alleviate H2O2-induced H9c2 cell apoptosis.PMID:36741296 | PMC:PMC9897913 | DOI:10.1155/2023/8141129
Source: Cardiology Research and Practice - February 6, 2023 Category: Cardiology Authors: Beibei Wang Jinsheng Zhang Aijun Xu Source Type: research

BRD4 Silencing Protects Angiotensin II-Induced Cardiac Hypertrophy by Inhibiting TLR4/NF- < em > κ < /em > B and Activating Nrf2-HO-1 Pathways
CONCLUSION: Our results speculate that the BRD4/TLR4 axis might be a promising strategy for treating cardiovascular diseases with cardiac hypertrophy, including HF.PMID:36247184 | PMC:PMC9553838 | DOI:10.1155/2022/8372707
Source: Cardiology Research and Practice - October 17, 2022 Category: Cardiology Authors: Ming Fang Jun Luo Xi Zhu Yingbiao Wu Xinming Li Source Type: research

The enigmatic role of VCAM-1 expressed by macrophages in mitochondrial metabolism and atherosclerosis
CONCLUSION: We conclude that macrophage-specific VCAM-1 augments mitochondrial biogenesis and DNA oxidation via Cmpk2. Oxidized mitochondrial DNA in plaque macrophages increases inflammation via Sting, resulting in exacerbation of atherosclerosis.PMID:35557156 | DOI:10.1096/fasebj.2022.36.S1.R6141
Source: Atherosclerosis - May 13, 2022 Category: Cardiology Authors: Niranjana Natarajan Jonathan Florentin Scott P O'Neil Lee L Ohayon Partha Dutta Source Type: research

Upregulation of Periostin Through CREB Participates in Myocardial Infarction-induced Myocardial Fibrosis
This study aims to verify the hypothesis that CREB promotes the expression of periostin in MI-induced myocardial fibrosis. To test this hypothesis, primary rat cardiac fibroblasts were cultured and rat model of MI was established. The level of myocardial fibrosis post-MI was identified by histological staining. The expressions of CREB and periostin were detected through western blot and reverse transcription quantity polymerase chain reaction. The upregulation and downregulation of CREB and periostin were established by plasmid, small interfere RNA (siRNA), and lentivirus, respectively. High levels of CREB and periostin we...
Source: Journal of Cardiovascular Pharmacology - May 1, 2022 Category: Cardiology Tags: Original Article Source Type: research

GSK-3 β Localizes to the Cardiac Z-Disc to Maintain Length Dependent Activation
CONCLUSIONS: We identified a novel mechanism by which GSK-3β localizes to the myofilament to modulate LDA. Importantly, z-disc GSK-3β levels were reduced in patients with heart failure, indicating z-disc localized GSK-3β is a possible therapeutic target to restore the Frank-Starling mechanism in patients with heart failure.PMID:35168370 | DOI:10.1161/CIRCRESAHA.121.319491
Source: Circulation Research - February 16, 2022 Category: Cardiology Authors: Marisa J Stachowski-Doll Maria Papadaki Thomas G Martin Weikang Ma Henry M Gong Stephanie Shao Shi Shen Nitha Aima Muntu Mohit Kumar Edith Perez Jody L Martin Christine S Moravec Sakthivel Sadayappan Stuart G Campbell Thomas Irving Jonathan A Kirk Source Type: research