ArticleRedox biology2018
Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Humanin improves bone health in a glucocorticoid-treated mouse model of Duchenne muscular dystrophy.Biochemistry and biophysics reports · 2026Article
- Role of Histone Deacetylase and Inhibitors in Cardiovascular Diseases.Cell proliferation · 2025Review
- Mammalian TatD DNase domain containing 1 (TATDN1) is a proteostasis-responsive gene with roles in ventricular structure and neuromuscular function.The FEBS journal · 2025Article
- A cardiac fibroblast-enriched micropeptide regulates inflammation in ischemia/reperfusion injury.JCI insight · 2025Article
- Mitochondria‑derived peptides: Promising microproteins in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- UPRmt-regulated mitokines: novel strategies for myocardial injury repair.Frontiers in cell and developmental biology · 2025Review
- Mitochondrial-derived peptides in cardiovascular disease: Novel insights and therapeutic opportunities.Journal of advanced research · 2024Review
- Reply to: The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria.Nature communications · 2024Article
- The effects of ENDOG on lipid metabolism may be tissue-dependent and may not require its translocation from mitochondria.Nature communications · 2024Article
- SIRT6 regulates obesity-induced oxidative stress via ENDOG/SOD2 signaling in the heart.Cell biology and toxicology · 2023Article
- Lethal effects of mitochondria via microfluidics.Bioengineering & translational medicine · 2023Article
- Proteomics analysis in myocardium of spontaneously hypertensive rats.Scientific reports · 2023Article
- Theoretical investigation on a simple turn on fluorescent probe for detection of biothiols based on coumarin unit.Frontiers in chemistry · 2023Article
- Shrimp miR-965 transfers tumoricidal mitochondria.Biological procedures online · 2022Article
- Anti-Diabetic Therapy, Heart Failure and Oxidative Stress: An Update.Journal of clinical medicine · 2022Review
- Cariporide Attenuates Doxorubicin-Induced Cardiotoxicity in Rats by Inhibiting Oxidative Stress, Inflammation and Apoptosis Partly Through Regulation of Akt/GSK-3β and Sirt1 Signaling Pathway.Frontiers in pharmacology · 2022Article
- Analysis of Therapeutic Targets of A Novel Peptide Athycaltide-1 in the Treatment of Isoproterenol-Induced Pathological Myocardial Hypertrophy.Cardiovascular therapeutics · 2022Article
- ENDOG Impacts on Tumor Cell Proliferation and Tumor Prognosis in the Context of PI3K/PTEN Pathway Status.Cancers · 2021Article
- Co-Exposure of Cardiomyocytes to IFN-γ and TNF-α Induces Mitochondrial Dysfunction and Nitro-Oxidative Stress: Implications for the Pathogenesis of Chronic Chagas Disease Cardiomyopathy.Frontiers in immunology · 2021Article
- Protective Mechanism of Humanin Against Oxidative Stress in Aging-Related Cardiovascular Diseases.Frontiers in endocrinology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endonuclease G gene (Endog), which codes for a mitochondrial nuclease, was identified as a determinant of cardiac hypertrophy. How ENDOG controls cardiomyocyte growth is still unknown. Thus, we aimed at finding the link between ENDOG activity and cardiomyocyte growth. Endog deficiency induced reactive oxygen species (ROS) accumulation and abnormal growth in neonatal rodent cardiomyocytes, altering the AKT-GSK3β and Class-II histone deacethylases (HDAC) signal transduction pathways. These effects were blocked by ROS scavengers. Lack of ENDOG reduced mitochondrial DNA (mtDNA) replication independently of ROS accumulation. Because mtDNA encodes several subunits of the mitochondrial electron transport chain, whose activity is an important source of cellular ROS, we investigated whether Endog deficiency compromised the expression and activity of the respiratory chain complexes but found no changes in these parameters nor in ATP content. MtDNA also codes for humanin, a micropeptide with possible metabolic functions. Nanomolar concentrations of synthetic humanin restored normal ROS levels and cell size in Endog-deficient cardiomyocytes. These results support the involvement of redox signaling in the control of cardiomyocyte growth by ENDOG and suggest a pathway relating mtDNA content to the regulation of cell growth probably involving humanin, which prevents reactive oxygen radicals accumulation and hypertrophy induced by Endog deficiency.
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