Sexually dimorphic effects of SARM1 deletion on cardiac NAD metabolism and function.

Nicotinamide adenine dinucleotide (NAD) decline is repeatedly observed in heart disease and its risk factors. Although strategies promoting NAD synthesis to elevate NAD levels improve cardiac function, whether inhibition of NAD consumption can be therapeutic is less investigated. In this study, we examined the role of sterile-α and TIR motif containing 1 (SARM1) NAD hydrolase in mouse hearts, using global SARM1-knockout mice (KO).

Paricalcitol Attenuates Metabolic Syndrome-Associated Heart Failure through Enhanced Mitochondrial Fusion.

Objectives: Transition from cardiac hypertrophy to failure involves adverse metabolic reprogramming involving mitochondrial dysfunction. We have earlier shown that vitamin D deficiency induces heart failure, at least in part, through insulin resistance. However, whether activation of vitamin D receptor (VDR) can attenuate heart failure and underlying metabolic phenotype requires investigation.

Harnessing NAD Metabolism as Therapy for Cardiometabolic Diseases.

Purpose Of The Review: This review summarizes current understanding on the roles of nicotinamide adenine dinucleotide (NAD) metabolism in the pathogeneses and treatment development of metabolic and cardiac diseases.

Recent Findings: NAD was identified as a redox cofactor in metabolism and a co-substrate for a wide range of NAD-dependent enzymes. NAD redox imbalance and depletion are associated with many pathologies where metabolism plays a key role, for example cardiometabolic diseases.

Activation of toll like receptor 4 (TLR4) promotes cardiomyocyte apoptosis through SIRT2 dependent p53 deacetylation.

Cardiomyocyte inflammation followed by apoptosis and fibrosis is an important mediator for development and progression of heart failure. Activation of toll-like receptor 4 (TLR4), an important regulator of inflammation, causes the progression of cardiac hypertrophy and injury. However, the precise mechanism of TLR4-mediated adverse cardiac outcomes is still elusive.

Fruit Rich in Polyphenols Attenuates Isoproterenol-Induced Cardiac Hypertrophy in Rats via Inhibition of Inflammation and Oxidative Stress.

Colla (Family: Musaceae), commonly known as banana and native to India and other parts of Asia, is very rich in nutritional value and has strong antioxidant potential. In the present study, we have developed (MB) fruit pulp powder and evaluated its cardioprotective effect in cardiac hypertrophy, which is often associated with inflammation and oxidative stress. An ultra-high-pressure liquid chromatography-mass spectrometer (UPLC-MS/MS) has been used for the detection and systematic characterization of the phenolic compounds present in fruit pulp.

Vitamin D Deficiency in Rats Causes Cardiac Dysfunction by Inducing Myocardial Insulin Resistance.

Scope: Cause-effect relationship between vitamin D deficiency and cardiometabolic abnormalities remains undefined. The aim is to investigate the role of vitamin D deficiency in cardiac failure, through possible involvement in myocardial insulin signaling.

Methods And Results: Male SD rats (n = 6) are fed a normal diet (Con), vitamin D-deficient diet [Con(-)], or high-fat, high fructose diet (HFHFrD) for 20 weeks.

Inhibition of SGLT1 abrogates preconditioning-induced cardioprotection against ischemia-reperfusion injury.

Background: Recently, we reported Na+/glucose co-transporter (SGLT1) expression in mouse and human heart. We speculated that SGLT1 might play an important role in ischemic preconditioning-induced cardioprotection. Therefore, the present study was designed to find the role of SGLT1 in ischemic preconditioning-induced cardioprotection.