ArticleMolecular medicine reports2018
N‑terminal truncated peroxisome proliferator‑activated receptor‑γ coactivator‑1α alleviates phenylephrine‑induced mitochondrial dysfunction and decreases lipid droplet accumulation in neonatal rat cardiomyocytes.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Cold-induced expression of a truncated adenylyl cyclase 3 acts as rheostat to brown fat function.Nature metabolism · 2024Article
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- Lipid Droplet-a New Target in Ischemic Heart Disease.Journal of cardiovascular translational research · 2022Review
- Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021Review
- Activation of calcium‑sensing receptor‑mediated autophagy in high glucose‑induced cardiac fibrosis in vitro.Molecular medicine reports · 2020Article
- Alterations in gut microbiota of abdominal aortic aneurysm mice.BMC cardiovascular disorders · 2020Article
- PPARα contributes to protection against metabolic and inflammatory derangements associated with acute kidney injury in experimental sepsis.Physiological reports · 2019Article
- COX6B1 relieves hypoxia/reoxygenation injury of neonatal rat cardiomyocytes by regulating mitochondrial function.Biotechnology letters · 2019Article
- A CRM1 Inhibitor Alleviates Cardiac Hypertrophy and Increases the Nuclear Distribution of NT-PGC-1α in NRVMs.Frontiers in pharmacology · 2019Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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