ArticleMolecular medicine (Cambridge, Mass.)2014
Resveratrol restores sirtuin 1 (SIRT1) activity and pyruvate dehydrogenase kinase 1 (PDK1) expression after hemorrhagic injury in a rat model.
Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- The structure and function of taste G protein-coupled receptors and their implications in diseases.International journal of oral science · 2026Review
- Resveratrol Impairs Insulin Signaling in Hepatic Cells via Activation of PKC and PTP1B Pathways.International journal of molecular sciences · 2025Article
- Curcumin and EGCG combined formulation in nanostructured lipid carriers for anti-aging applications.International journal of pharmaceutics: X · 2025Article
- Hemorrhagic Shock and Mitochondria: Pathophysiology and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Pyrroloquinoline quinone (PQQ) protects mitochondrial function of HEI-OC1 cells under premature senescence.npj aging · 2022Article
- Longevity pathways in stress resistance: targeting NAD and sirtuins to treat the pathophysiology of hemorrhagic shock.GeroScience · 2021Article
- Protein acetylation and deacetylation: An important regulatory modification in gene transcription (Review).Experimental and therapeutic medicine · 2020Review
- Deficiency of metabolite sensing receptor HCA2 impairs the salutary effect of niacin in hemorrhagic shock.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Epigenetic Regulatory Mechanisms Induced by Resveratrol.Nutrients · 2017Review
- Mitochondrial dysfunction in rat splenocytes following hemorrhagic shock.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Mitochondrial function in hypoxic ischemic injury and influence of aging.Progress in neurobiology · 2017Review
- Attenuation of Multiple Organ Damage by Continuous Low-Dose Solvent-Free Infusions of Resveratrol after Severe Hemorrhagic Shock in Rats.Nutrients · 2017Article
- 3-Phosphoinositide Dependent Protein Kinase-1 (PDK-1) Promotes Migration and Invasion in Gastric Cancer Cells Through Activating the NF-κB Pathway.Oncology research · 2017Article
- Mitochondrial targeting by dichloroacetate improves outcome following hemorrhagic shock.Scientific reports · 2017Article
- SIRT1 is required for mitochondrial biogenesis reprogramming in hypoxic human pulmonary arteriolar smooth muscle cells.International journal of molecular medicine · 2017Article
- Hemorrhagic shock-induced cerebral bioenergetic imbalance is corrected by pharmacologic treatment with EF24 in a rat model.Neuropharmacology · 2015Article
- Activation of sirtuin 1/3 improves vascular hyporeactivity in severe hemorrhagic shock by alleviation of mitochondrial damage.Oncotarget · 2015Article
- Sirtuin regulation in aging and injury.Biochimica et biophysica acta · 2015Review
- Oxidative stress response and Nrf2 signaling in aging.Free radical biology & medicine · 2015Review
- Polydatin Alleviates Small Intestine Injury during Hemorrhagic Shock as a SIRT1 Activator.Oxidative medicine and cellular longevity · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Severe hemorrhage leads to decreased blood flow to tissues resulting in decreased oxygen and nutrient availability affecting mitochondrial function. A mitoscriptome profiling study demonstrated alteration in several genes related to mitochondria, consistent with the mitochondrial functional decline observed after trauma hemorrhage (T-H). Our experiments led to the identification of sirtuin 1 (SIRT1) as a potential target in T-H. Administration of resveratrol (a naturally occurring polyphenol and activator of SIRT1) after T-H improved left ventricular function and tissue ATP levels. Our hypothesis was that mitochondrial function after T-H depends on SIRT1 activity. In this study, we evaluated the activity of SIRT1, a mitochondrial functional modulator, and the mitochondrial-glycolytic balance after T-H. We determined the changes in protein levels of pyruvate dehydrogenase kinase (PDK)-1 and nuclear c-Myc, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and NF-E2-related factor (NRF)2 after T-H and after treatment with resveratrol or a combination of sirtinol (a SIRT1 inhibitor) and resveratrol. We have also tested the activity of mitochondrial complex 1. SIRT1 enzyme activity was significantly decreased after T-H, whereas resveratrol treatment restored the activity. We found elevated PDK1 and c-Myc levels and decreased PGC-1α, NRF2 and mitochondrial complex I activity after T-H. The reduced SIRT1 activity after T-H may be related to declining mitochondrial function, since resveratrol was able to reinstate SIRT1 activity and mitochondrial function. The elevated level of PDK1 (an inhibitor of pyruvate dehydrogenase complex) after T-H indicates a possible shift in cellular energetics from mitochondria to glycolysis. In conclusion, SIRT1 modulation alters left ventricular function after T-H through regulation of cellular energetics.
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