Qingchun Zeng

N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes

N-terminal truncated peroxisome proliferator-activated receptor-γ coactivator-1α (NT-PGC-1α) is an alternative splice variant of PGC-1α. NT-PGC-1α exhibits stronger anti-obesity effects in adipose tissue than PGC-1α; however, NT-PGC-1α has not yet been investigated in neonatal rat cardiomyocytes (NRCMs). The present study aimed to investigate the role of NT-PGC-1α in mitochondrial fatty acid metabolism and its possible regulatory mechanism in NRCMs. NRCMs were exposed to phenylephrine (PE) or angiotensin II (Ang II) to induce cardiac hypertrophy. Following this, NRCMs were infected with adenovirus expressing NT-PGC-1α, and adenosine 5′-triphsophate (ATP) levels, reactive oxygen species (ROS) generation and mitochondrial membrane potential were subsequently detected. In addition, western blotting, lipid droplet staining and oxygen consumption assays were performed to examine the function of NT-PGC-1α in fatty acid metabolism. NT-PGC-1α was demonstrated to be primarily expressed in the cytoplasm, which differed from full-length PGC-1α, which was predominantly expressed in the nucleus. NT-PGC-1α overexpression alleviated mitochondrial function impairment, including ATP generation, ROS production and mitochondrial membrane potential integrity. Furthermore, NT-PGC-1α overexpression alleviated the PE-induced suppression of fatty acid metabolism-associated protein expression, increased extracellular oxygen consumption and decreased lipid droplet accumulation in NRCMs. Taken together, the present study demonstrated that NT-PGC-1α alleviated PE-induced mitochondrial impairment and decreased lipid droplet accumulation in NRCMs, indicating that NT-PGC-1α may have ameliorated mitochondrial energy defects in NRCMs, and may be considered as a potential target for the treatment of heart failure.

GW29-e0367 PTEN Induced Putative Kinase 1 (PINK1) Regulates Mitophagy to Alleviate Angiotensin II-Induced Cardiac Injury

Angiotensin Ⅱ (Ang Ⅱ)-induced cardiac injury can result in elevated oxidative stress and decreased mitochondrial quality. Meanwhile, PTEN induced putative kinase 1 (PINK1) participate in mitochondrial quality control. However, the mechanism of PINK1 in Ang Ⅱ-induced cardiac injury remain

GW28-e0577 Trimethylamine-N-oxide induces the osteogenic responses of human aortic valve interstitisl cells through the endoplasmic reticulum-mitochondrial stress pathways

The recent studies show that the choline-derived metabolite trimethylamine N-oxide (TMAO) levels are associated with the development of cardiovascular diseases. TMAO causesxa0cell inflammation and endoplasmic reticulum stress. Inflammatory responses and endoplasmic reticulum stress are involved in

GW28-e0651 Association between homocysteine levels and calcific aortic valve disease: a meta-analysis

Previous studies have reported inconsistent results regarding the association between homocysteine (Hcy) levels and calcific aortic valve disease (CAVD). This study aims to investigate the association between Hcy levels in patients with CAVD by conducting a meta-analysis.nnWe conducted a systematic

The top tertile of hematocrit change during hospitalization is associated with lower risk of mortality in acute heart failure patients

BackgroundHemoconcentration has been proposed as surrogate for changes in volume status among patients hospitalized with acute heart failure (AHF) and is associated with a favorable outcome. However, there is a dearth of research assessing the clinical outcomes of hospitalized patients with hemoconcentration, hemodilution and unchanged volume status.MethodsWe enrolled 510 consecutive patients hospitalized for AHF from April 2011 to July 2015. Hematocrit (HCT) levels were measured at admission and either at discharge or on approximately the seventh day of admission. Patients were stratified by delta HCT tertitles into hemodilution (ΔHCT ≤xa0−xa01.6%), no change (NC, −1.6%xa0<xa0ΔHCT ≤1.5%) and hemoconcentration (ΔHCT >1.5%) groups. The endpoint was all-cause death, with a median follow-up duration of 18.9xa0months.ResultsHemoconcentration was associated with lower left ventricle ejection fraction, as compared with NC and hemodilution groups, while renal function at entry, New York Heart Association class IV, and in-hospital worsening renal function (WRF) were not significantly different across the three groups. After multivariable adjustment, hemoconcentration had a lower risk of mortality as compared with hemodilution [hazard ratio (HR) 0.39, 95% confidence interval (CI) 0.24–0.63, Pxa0<xa00.001], or NC (HR 0.54, 95% CI 0.33–0.88, Pxa0=xa00.015], while hemodilution and NC did not have significantly differ in mortality (HR 0.72, 95% CI 0.48–1.10, Pxa0=xa00.130).ConclusionsIn patients hospitalized with AHF, an increased HCT during hospitalization is associated with a lower risk of all-cause mortality than a decreased or unchanged HCT. Furthermore, all-cause mortality does not differ significantly between patients with unchanged and decreased HCT values.

Association between homocysteine levels and calcific aortic valve disease: a systematic review and meta-analysis

Previous studies have reported inconsistent results regarding the association between homocysteine (Hcy) levels and calcific aortic valve disease (CAVD). We investigate the association between Hcy levels in patients with CAVD and controls by conducting a systematic review and meta-analysis. We conducted a systematic search of studies published prior to the end of March 2017 in the PubMed, Embase, Web of Science, Cochrane Central Register of Controlled Trials and the Chinese Biomedical Literature databases. Eligible studies evaluating plasma Hcy levels in CAVD patients and controls were identified by two independent investigators. Standardized mean difference (SMD) and the corresponding 95% confidence intervals (95% CIs) were estimated using the random-effects model. Ten studies involving 6349 participants were included. Pooled analysis demonstrated that Hcy levels were significantly elevated in patients with CAVD compared with controls (pooled SMD: 0.57, 95% CI: 0.36–0.79). This elevation was more obvious in American and Asian populations than in Turkish populations. Furthermore, Hcy levels were significantly elevated in patients with mild-to-moderate CAVD and severe CAVD. Our results demonstrate that CAVD is associated with elevated Hcy levels.