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Benefits of Curcumin in the Vasculature: A Therapeutic Candidate for Vascular Remodeling in Arterial Hypertension and Pulmonary Arterial Hypertension?
Growing evidence suggests that hypertension is one of the leading causes of cardiovascular morbidity and mortality since uncontrolled high blood pressure increases the risk of myocardial infarction, aortic dissection, hemorrhagic stroke, and chronic kidney disease. Impaired vascular homeostasis plays a critical role in the development of hypertension-induced vascular remodeling. Abnormal behaviors of vascular cells are not only a pathological hallmark of hypertensive vascular remodeling, but also an important pathological basis for maintaining reduced vascular compliance in hypertension. Targeting vascular remodeling repre...
Source: Frontiers in Physiology - April 1, 2022 Category: Physiology Source Type: research

Deficiency of Ataxia-Telangiectasia Mutated Kinase Modulates Functional and Biochemical Parameters of the Heart in Response to Western-type Diet
Am J Physiol Heart Circ Physiol. 2021 Apr 30. doi: 10.1152/ajpheart.00990.2020. Online ahead of print.ABSTRACTAtaxia telangiectasia mutated kinase (ATM) deficiency exacerbates heart dysfunction late after myocardial infarction. Here, we hypothesized that ATM deficiency modulates Western-type diet (WD)-induced cardiac remodeling with an emphasis on functional and biochemical parameters of the heart. Weight gain was assessed in male wild-type (WT) and ATM heterozygous knockout (hKO) mice on weekly basis, while cardiac functional and biochemical parameters were measured 14 weeks post-WD. hKO-WD mice exhibited rapid body weigh...
Source: American Journal of Physiology. Heart and Circulatory Physiology - April 30, 2021 Category: Physiology Authors: Mary C Wingard Suman Dalal Paige L Shook Rachel Myers Barbara A Connelly Douglas P Thewke Mahipal Singh Krishna Singh Source Type: research

Impaired Activity of Ryanodine Receptors Contributes to Calcium Mishandling in Cardiomyocytes of Metabolic Syndrome Rats
Conclusion Principal findings of this work are that abnormal Ca2+ transient amplitude, contractile dysfunction; and impaired relaxation of MetS cardiomyocytes underlies intrinsic dysfunctional RyR2 and SERCA pump. Abnormal activity of RyRs was evidenced by its decreased ability to bind [3H]-ryanodine. Although the MetS condition does not modify RyR2 protein expression, its phosphorylation at Ser2814 is decreased, which impairs its capacity for activation during ECC. The dysfunctional RyRs, together with a decreased activity of SERCA pump due to decreased Thr17-PLN phosphorylation suggest a downregulation of CaMKII in MetS...
Source: Frontiers in Physiology - April 29, 2019 Category: Physiology Source Type: research