ArticleThe Journal of biological chemistry2010
PGC-1 alpha serine 570 phosphorylation and GCN5-mediated acetylation by angiotensin II drive catalase down-regulation and vascular hypertrophy.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 82 citations in OpenAlex.
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- Revisiting ROS: duality in organ aging progression.Molecular biology reports · 2025Review
- Review
- Levocarnitine improves cardiac energy metabolic remodeling in myocarditis mice.Frontiers in pharmacology · 2025Article
- Targeting catalase in cancer.Redox biology · 2024Review
- Curculigoside Attenuates Endoplasmic Reticulum Stress-Induced Epithelial Cell and Fibroblast Senescence by Regulating the SIRT1-P300 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms.Molecular biology reports · 2024Review
- Connecting epigenetics and inflammation in vascular senescence: state of the art, biomarkers and senotherapeutics.Frontiers in genetics · 2024Review
- Mitochondrial Homeostasis in VSMCs as a Central Hub in Vascular Remodeling.International journal of molecular sciences · 2023Review
- Losartan Mitigates Oxidative Stress in the Brains of Aged and Inflamed IL-10-/- Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Article
- Thioredoxin Prevents Loss of UCP2 in Hyperoxia via MKK4-p38 MAPK-PGC1α Signaling and Limits Oxygen Toxicity.American journal of respiratory cell and molecular biology · 2022Article
- Role of angiotensin II in aging.Frontiers in aging neuroscience · 2022Review
- PTEN loss promotes Warburg effect and prostate cancer cell growth by inducing FBP1 degradation.Frontiers in oncology · 2022Article
- The mechanisms of vascular aging.Aging medicine (Milton (N.S.W)) · 2021Review
- Article
- KLF5 Is Induced by FOXO1 and Causes Oxidative Stress and Diabetic Cardiomyopathy.Circulation research · 2021Article
- GCN5 acetyltransferase in cellular energetic and metabolic processes.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021Review
- PGC-1Oxidative medicine and cellular longevity · 2021Article
- Cardiac Fibroblast-Specific Knockout of PGC-1α Accelerates AngII-Induced Cardiac Remodeling.Frontiers in cardiovascular medicine · 2021Article
- Urinary Metabolomic Profiling in Streptozotocin-Induced Diabetic Mice after Treatment with Losartan.International journal of molecular sciences · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Angiotensin II (Ang II) is a pleuripotential hormone that is important in the pathophysiology of multiple conditions including aging, cardiovascular and renal diseases, and insulin resistance. Reactive oxygen species (ROS) are important mediators of Ang II-induced signaling generally and have a well defined role in vascular hypertrophy, which is inhibited by overexpression of catalase, inferring a specific role of H(2)O(2). The molecular mechanisms are understood incompletely. The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) is a key regulator of energy metabolism and ROS-scavenging enzymes including catalase. We show that Ang II stimulates Akt-dependent PGC-1 alpha serine 570 phosphorylation, which is required for the binding of the histone acetyltransferase GCN5 (general control nonderepressible 5) to PGC-1 alpha and for its lysine acetylation. These sequential post-translational modifications suppress PGC-1 alpha activity and prevent its binding to the catalase promoter through the forkhead box O1 transcription factor, thus decreasing catalase expression. We demonstrate that overexpression of the phosphorylation-defective mutant PGC-1 alpha (S570A) prevents Ang II-induced increases in H(2)O(2) levels and hypertrophy ([(3)H]leucine incorporation). Knockdown of PGC-1 alpha by small interfering RNA promotes basal and Ang II-stimulated ROS and hypertrophy, which is reversed by polyethylene glycol-conjugated catalase. Thus, endogenous PGC-1 alpha is a negative regulator of vascular hypertrophy by up-regulating catalase expression and thus reducing ROS levels. We provide novel mechanistic insights by which Ang II may mediate its ROS-dependent pathophysiologic effects on multiple cardiometabolic diseases.
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