ArticleOncotarget2015
Activation of sirtuin 1/3 improves vascular hyporeactivity in severe hemorrhagic shock by alleviation of mitochondrial damage.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Blocking mitochondrial cyclophilin D ameliorates TSH-impaired defensive barrier of artery.Redox biology · 2018Trial
- Identification and validation of a novel mitochondrion-related gene signature for diagnosis and immune infiltration in sepsis.Frontiers in immunology · 2023Article
- The mitochondrial permeability transition: Recent progress and open questions.The FEBS journal · 2022Review
- Review
- Pyrroloquinoline quinone (PQQ) protects mitochondrial function of HEI-OC1 cells under premature senescence.npj aging · 2022Article
- Renalase Challenges the Oxidative Stress and Fibroproliferative Response in COVID-19.Oxidative medicine and cellular longevity · 2022Review
- Sirtuins and Sepsis: Cross Talk between Redox and Epigenetic Pathways.Antioxidants (Basel, Switzerland) · 2021Review
- Longevity pathways in stress resistance: targeting NAD and sirtuins to treat the pathophysiology of hemorrhagic shock.GeroScience · 2021Article
- Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways.Cell death & disease · 2020Article
- Polydatin protects against lipopolysaccharide-induced endothelial barrier disruption via SIRT3 activation.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Article
- Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation.Oxidative medicine and cellular longevity · 2020Article
- Mitochondrial Dysfunction: Metabolic Drivers of Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this mapReview
- Regulation of Sirtuin 3-Mediated Deacetylation of Cyclophilin D Attenuated Cognitive Dysfunction Induced by Sepsis-Associated Encephalopathy in Mice.Cellular and molecular neurobiology · 2017Article
- Review
- Attenuation of Multiple Organ Damage by Continuous Low-Dose Solvent-Free Infusions of Resveratrol after Severe Hemorrhagic Shock in Rats.Nutrients · 2017Article
- SIRT1 is required for mitochondrial biogenesis reprogramming in hypoxic human pulmonary arteriolar smooth muscle cells.International journal of molecular medicine · 2017Article
- SIRT1/3 Activation by Resveratrol Attenuates Acute Kidney Injury in a Septic Rat Model.Oxidative medicine and cellular longevity · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular hyporeactivity is one of the major causes responsible for refractory hypotension and associated mortality in severe hemorrhagic shock. Mitochondrial permeability transition (mPT) pore opening in arteriolar smooth muscle cells (ASMCs) is involved in the pathogenesis of vascular hyporeactivity. However, the molecular mechanism underlying mitochondrial injury in ASMCs during hemorrhagic shock is not well understood. Here we produced an in vivo model of severe hemorrhagic shock in adult Wistar rats. We found that sirtuin (SIRT)1/3 protein levels and deacetylase activities were decreased in ASMCs following severe shock. Immunofluorescence staining confirmed reduced levels of SIRT1 in the nucleus and SIRT3 in the mitochondria, respectively. Acetylation of cyclophilin D (CyPD), a component of mPT pore, was increased. SIRT1 activators suppressed mPT pore opening and ameliorated mitochondrial injury in ASMCs after severe shock. Furthermore, administration of SIRT1 activators improved vasoreactivity in rats under severe shock. Our data suggest that epigenetic mechanisms, namely histone post-translational modifications, are involved in regulation of mPT by SIRT1/SIRT3- mediated deacetylation of CyPD. SIRT1/3 is a promising therapeutic target for the treatment of severe hemorrhagic shock.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.