Carnitine Palmitoyltransferase-1b Deficiency Aggravates Pressure Overload–Induced Cardiac Hypertrophy Caused by Lipotoxicity
CPT1b deficiency can cause lipotoxicity in the heart under pathological stress, leading to exacerbation of cardiac pathology, and caution should be exercised in the clinical use of CPT1 inhibitors.
Cardiomyocyte-Specific BMAL1 Plays Critical Roles in Metabolism, Signaling, and Maintenance of Contractile Function of the Heart
Studies reveal that BMAL1 influences metabolism, signaling, and contractile function of the heart, and reveals age-onset development of dilated cardiomyopathy in CBK mice, associated with a severe reduction in life span.
Stromal interaction molecule 1 is essential for normal cardiac homeostasis through modulation of ER and mitochondrial function.
It is demonstrated for the first time that STIM1 plays an essential role in normal cardiac function in the adult heart, which may be important for the regulation of ER and mitochondrial function.
Peroxisome Proliferator-Activated Receptor &bgr;/&dgr; Activation in Adult Hearts Facilitates Mitochondrial Function and Cardiac Performance Under Pressure-Overload Condition
It is concluded that PPAR&bgr;/&dgr; activation in the adult heart will promote cardiac performance along with transcriptional upregulation of mitochondrial biogenesis and defense, as well as oxidative metabolism at basal and pressure-overload conditions.
Cardiomyocyte-Restricted Deletion of PPARβ/δ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation
It is demonstrated that cardiomyocyte-restricted deletion of PPARβ/δ in PPARα-null mice causes impaired mitochondrial biogenesis and defense, but no further depression of fatty acid oxidation.
Live cell screening platform identifies PPARδ as a regulator of cardiomyocyte proliferation and cardiac repair
A cardiomyocyte proliferation screening system is established and a new drugable target with promise for the treatment of cardiac pathologies caused by cardiomeocyte loss is presented.
Altered myocardial metabolic adaptation to increased fatty acid availability in cardiomyocyte-specific CLOCK mutant mice.
Carnitine Palmitoyltransferase 1b Deficiency Protects Mice from Diet-Induced Insulin Resistance
The present study on a genetic model of Cpt1b restriction supports the concept that partial CPT1b inhibition is a potential therapeutic strategy against type II diabetes.
Biotinylation: a novel posttranslational modification linking cell autonomous circadian clocks with metabolism.
Expiration of the biotin transporter slc5a6 gene is decreased in hearts of two distinct genetic mouse models of cardiomyocyte-specific circadian clock disruption and biotinylation is a novel mechanism by which cell autonomous circadian clocks influence metabolic pathways.
Carnitine Palmitoyltransferase-1 b ( CPT 1 b ) Deficiency Aggravates Pressure-Overload-Induced Cardiac Hypertrophy due to Lipotoxicity
Background-Carnitine palmitoyltransferase 1(CPT1) is a rate-limiting step of mitochondrial E and deficiency aggravates pressure-overload-induced cardiac hypertrophy.