Diabetes is a risk factor that increases the occurrence and severity of cardiovascular events. Cardiovascular complications are the leading cause of mortality of 75% of patients with diabetes >40 years old. Sesamin, the bioactive compound extracted from Sesamum indicum, is a natural compound that has diverse beneficial effects on hypoglycemia and reducing cholesterol. The aim of this study is to investigate sesamin effects to diabetes-inducing cardiac hypertrophy. In the present study bioinformatics analysis demonstrated cardiac hypertrophy signaling may be the most important pathway for upregulating genes in sesamin-treated groups. To verify the bioinformatics prediction, sesamin was used as the main bioactive compound to attenuate the impact of diabetes induced by streptozotocin (STZ) on cardiac function in a rat model. The results revealed that oral administration of sesamin for 4 weeks (100 and 200 mg/kg body weight) marginally improved blood glucose levels, body weight and significantly ameliorated the effects on heart rate and blood pressure in rats with type 1 diabetes relative to control rats. The QT interval of sesamin was also reduced relative to the control group. The findings indicated that sesamin has potential cardioprotective effects in the STZ-induced diabetes model. This suggested that this can be used as a novel treatment for patients with diabetes with cardiac dysfunction complication.
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http://dx.doi.org/10.3892/mmr.2017.6420 | DOI Listing |
J Transl Med
January 2025
Aerospace Medical Center, Aerospace Center Hospital, Beijing, China.
Heart-on-a-chip (HoC) devices have emerged as a powerful tool for studying the human heart's intricate functions and dysfunctions in vitro. Traditional preclinical models, such as 2D cell cultures model and animal model, have limitations in accurately predicting human response to cardiovascular diseases and treatments. The HoC approach addresses these shortcomings by recapitulating the microscale anatomy, physiology, and biomechanics of the heart, thereby providing a more clinically relevant platform for drug testing, disease modeling, and personalized therapy.
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January 2025
Department of Intensive Care Medicine, Army Medical Center of PLA, No. 10 Changjiang Road, Yuzhong District, Chongqing, 400010, People's Republic of China.
Background: Pregnancy-associated atypical hemolytic uremic syndrome (aHUS) is a form of thrombotic microangiopathy (TMA) caused by uncontrolled activation of the complement system during pregnancy or the postpartum period. In the intensive care unit, aHUS must be differentiated from sepsis-related multiple organ dysfunction, thrombotic thrombocytopenic purpura (TTP), hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. Early recognition of aHUS is critical for effective treatment and improved prognosis.
View Article and Find Full Text PDFBMC Pregnancy Childbirth
January 2025
Royal Hospital for Women and UNSW, School of Clinical Medicine, Level 0, Royal Hospital for Women, Barker Street (Locked Bag 2000), Sydney, NSW, 2031, Australia.
Background: Congenital heart disease (CHD) is the most common fetal malformation, and it can result first in cardiac remodeling and dysfunction and later in cardiac failure and hydrops. A limited number of studies have evaluated cardiac function in fetuses affected by CHD. Functional parameters could potentially identify fetuses at risk of cardiac failure before its development.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Pharmacology and Experimental Therapeutics; MS 1015, College of Pharmacy and Pharmaceutical Sciences, The University of Toledo, Health Education Building; Room 282E, 3000 Arlington Ave, Toledo, OH, 43614, USA.
We previously demonstrated that the inability of primary endothelial cilia to sense fluid shear stress can lead to nitric oxide (NO) deficiency and cause hypertension (HTN). Decreased biosynthesis of NO contributes to cerebral amyloid angiopathy in Alzheimer's disease (AD) patients through increased deposition of amyloid beta (Aβ). However, the molecular mechanisms underlying the pathogenesis of HTN and AD are incompletely understood.
View Article and Find Full Text PDFNat Commun
January 2025
Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California, CA, USA.
Myocardial fibrosis leads to cardiac dysfunction and arrhythmias in heart failure with preserved ejection fraction (HFpEF), but the underlying mechanisms remain poorly understood. Here, RNA sequencing identifies Forkhead Box1 (FoxO1) signaling as abnormal in male HFpEF hearts. Genetic suppression of FoxO1 alters the intercellular communication between cardiomyocytes and fibroblasts, alleviates abnormal diastolic relaxation, and reduces arrhythmias.
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