An unexpected interaction between diabetes and cardiovascular diseases on cognitive function: A cross-sectional study.

Objective: Impaired cognitive function in older individuals significantly affects quality of life. The interaction between comorbid diabetes and cardiovascular disease (CVD) and its impact on cognitive impairment remains unclear.

Methods: This study analyzed 2564 subjects from the National Health and Nutrition Examination Survey dataset.

Targeting WWP1 ameliorates cardiac ischemic injury by suppressing KLF15-ubiquitination mediated myocardial inflammation.

Previous studies have suggested that myocardial inflammation plays a critical role after ischemic myocardial infarction (MI); however, the underlying mechanisms still need to be fully elucidated. WW domain-containing ubiquitin E3 ligase 1 (WWP1) is considered as an important therapeutic target for cardiovascular diseases due to its crucial function in non-ischemic cardiomyopathy, though it remains unknown whether targeting WWP1 can alleviate myocardial inflammation and ischemic injury post-MI. Recombinant adeno-associated virus 9 (rAAV9)-cTnT-mediated WWP1 or Kruppel-like factor 15 (KLF15) gene transfer and a natural WWP1 inhibitor Indole-3-carbinol (I3C) were used to determine the WWP1 function in cardiomyocytes.

Ergosterol Attenuates Isoproterenol-Induced Myocardial Cardiotoxicity.

Phytomedicine has shown a promising potential for the prevention of cardiovascular system diseases and disorders. This study aimed to evaluate protective effect of ergosterol (ER) on isoproterenol (ISO)-induced myocardial cardiotoxicity. We found that pretreatment with ER significantly decreased levels of myocardial CK-MB and LDH, and alleviated myocardial damage induced by ISO in rat model.

The TIR/BB-loop mimetic AS-1 prevents Ang II-induced hypertensive cardiac hypertrophy via NF-κB dependent downregulation of miRNA-143.

Untreated pathological cardiac hypertrophy, which can be caused by sustained systemic hypertension, may lead to heart failure. In the present study, we investigated whether AS-1 had attenuating effects on hypertension-induced cardiac hypertrophy, and whether this process was mediated by the regulation of miRNA-143. To induce the hypertrophic response in vitro, cardiomyocytes were stimulated with Ang II for 24hs.