Monocarboxylate transporter 4 inhibition potentiates hepatoc... : Hepatology
Monocarboxylate transporter 4 inhibition potentiates hepatocellular carcinoma …

In hypertrophied and failing hearts, fuel metabolism is reprogrammed to increase glucose
metabolism, especially glycolysis. This metabolic shift favors biosynthetic function at the …

Background: Pathological cardiac hypertrophy is one of the leading causes of heart failure
with highly complicated pathogeneses. The E3 ligase TRIM16 (tripartite motif–containing …

Background: Cellular redox control is maintained by generation of reactive oxygen/nitrogen
species balanced by activation of antioxidative pathways. Disruption of redox balance leads …

Insulin receptors are highly expressed in the heart and vasculature. Insulin signaling
regulates cardiac growth, survival, substrate uptake, utilization, and mitochondrial …

Voltage dependent anion channel 2 (VDAC2) is an outer mitochondrial membrane porin
known to play a significant role in apoptosis and calcium signaling. Abnormalities in calcium …

The myocardium is capable of utilizing different energy substrates, which is referred to as
“metabolic flexibility.” This process assures ATP production from fatty acids, glucose, lactate …

The main hallmark of myocardial substrate metabolism in cardiac hypertrophy or heart
failure is a shift from fatty acid oxidation to greater reliance on glycolysis. However, the close …

Precise metabolic rewiring during heart organogenesis underlies normal cardiac
development. Herein, we utilized high-coverage, quantitative lipidomic approaches to …

As key organelles involved in cellular metabolism, mitochondria frequently undergo
adaptive changes in morphology, components and functions in response to various …