ArticlePloS one2012
A cardiac-specific robotized cellular assay identified families of human ligands as inducers of PGC-1α expression and mitochondrial biogenesis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Estradiol-PGC-1 signaling in mitochondrial health: Implications for perimenopause and cardiovascular disease.Physiological reports · 2026Review
- Molecular regulation of PGC-1α: from protein-protein interactions and post-translational modifications to pharmacological modulation.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Cardiac-Derived ECM Microspheres for Enhanced hiPSC-CMs Maturation.Advanced functional materials · 2026Article
- Expression profiles of histone H4K20 methylation and its associated enzymes in mouse cardiac disease and human heart failure.Epigenetics · 2025Article
- Complete Immunophenotypic Reversal of Chronic Lymphocytic Leukaemia With High Dose Parenteral Methylcobalamin: A Case Report and Brief Review of Cobalamin in Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- Cardiac Differentiation Promotes Focal Adhesions Assembly through Vinculin Recruitment.International journal of molecular sciences · 2023Article
- Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?International journal of molecular sciences · 2021Review
- Protease Inhibitor Anti-HIV, Lopinavir, Impairs Placental Endocrine Function.International journal of molecular sciences · 2021Article
- The Main Metabolites of Fluorouracil + Adriamycin + Cyclophosphamide (FAC) Are Not Major Contributors to FAC Toxicity in H9c2 Cardiac Differentiated Cells.Biomolecules · 2019Article
- Mitochondrial regulator PGC-1a-Modulating the modulator.Current opinion in endocrine and metabolic research · 2019Article
- Doxorubicin Is Key for the Cardiotoxicity of FAC (5-Fluorouracil + Adriamycin + Cyclophosphamide) Combination in Differentiated H9c2 Cells.Biomolecules · 2019Article
- Histone methyltransferase Smyd1 regulates mitochondrial energetics in the heart.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Pixantrone, a new anticancer drug with the same old cardiac problems? An in vitro study with differentiated and non-differentiated H9c2 cells.Interdisciplinary toxicology · 2018Article
- Small molecule PGC-1α1 protein stabilizers induce adipocyte Ucp1 expression and uncoupled mitochondrial respiration.Molecular metabolism · 2018Article
- Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia.Disease models & mechanisms · 2017Article
- Synergism between PGC-1α and estrogen in the survival of endometrial cancer cells via the mitochondrial pathway.OncoTargets and therapy · 2016Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMitochondrial function is dramatically altered in heart failure (HF). This is associated with a decrease in the expression of the transcriptional coactivator PGC-1α, which plays a key role in the coordination of energy metabolism. Identification of compounds able to activate PGC-1α transcription could be of future therapeutic significance. METHODOLOGY/PRINCIPAL
findingsWe thus developed a robotized cellular assay to screen molecules in order to identify new activators of PGC-1α in a cardiac-like cell line. This screening assay was based on both the assessment of activity and gene expression of a secreted luciferase under the control of the human PGC-1α promoter, stably expressed in H9c2 cells. We screened part of a library of human endogenous ligands and steroid hormones, B vitamins and fatty acids were identified as activators of PGC-1α expression. The most responsive compounds of these families were then tested for PGC-1α gene expression in adult rat cardiomyocytes. These data highly confirmed the primary screening, and the increase in PGC-1α mRNA correlated with an increase in several downstream markers of mitochondrial biogenesis. Moreover, respiration rates of H9c2 cells treated with these compounds were increased evidencing their effectiveness on mitochondrial biogenesis. CONCLUSIONS/SIGNIFICANCE: Using our cellular reporter assay we could identify three original families, able to activate mitochondrial biogenesis both in cell line and adult cardiomyocytes. This first screening can be extended to chemical libraries in order to increase our knowledge on PGC-1α regulation in the heart and to identify potential therapeutic compounds able to improve mitochondrial function in HF.
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