ArticleAmerican journal of respiratory cell and molecular biology2023
SIRT3 Is a Critical Regulator of Mitochondrial Function of Fibroblasts in Pulmonary Hypertension.
Article in American journal of respiratory cell and molecular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Advances in the Role of SIRT3 in Vascular Remodeling in Hypertension.Biomolecules · 2026Review
- Alisol A Mitigates Neuroinflammation and Oxidative Stress After Subarachnoid Hemorrhage Through SIRT3-Driven Reprogramming of Mitochondrial Metabolism.Molecular neurobiology · 2026Article
- Adventitial fibroblasts direct smooth muscle cell-state transition in pulmonary vascular disease.eLife · 2025Article
- Honokiol and Nicotinamide Adenine Dinucleotide Improve Exercise Endurance in Pulmonary Hypertensive Rats Through Increasing SIRT3 Function in Skeletal Muscle.International journal of molecular sciences · 2024Article
- Selenium supplementation elevated SELENBP1 to inhibit fibroblast activation in pulmonary arterial hypertension.iScience · 2024Article
- Review
- Article
- Bawei Chenxiang Wan ameliorates right ventricular hypertrophy in rats with high altitude heart disease by SIRT3-HIF1α-PDK/PDH signaling pathway improving fatty acid and glucose metabolism.BMC complementary medicine and therapies · 2024Article
- Repetitive sulfur dioxide exposure in mice models post-deployment respiratory syndrome.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Boosting the Exhausted Vasculature-SIRT3 (to the) Rescue.American journal of respiratory cell and molecular biology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Pulmonary hypertension (PH) is a heterogeneous and life-threatening cardiopulmonary disorder in which mitochondrial dysfunction is believed to drive pathogenesis, although the underlying mechanisms remain unclear. To determine if abnormal SIRT3 (sirtuin 3) activity is related to mitochondrial dysfunction in adventitial fibroblasts from patients with idiopathic pulmonary arterial hypertension (IPAH) and hypoxic PH calves (PH-Fibs) and whether SIRT3 could be a potential therapeutic target to improve mitochondrial function, SIRT3 concentrations in control fibroblasts, PH-Fibs, and lung tissues were determined using quantitative real-time PCR and western blot. SIRT3 deacetylase activity in cells and lung tissues was determined using western blot, immunohistochemistry staining, and immunoprecipitation. Glycolysis and mitochondrial function in fibroblasts were measured using respiratory analysis and fluorescence-lifetime imaging microscopy. The effects of restoring SIRT3 activity (by overexpression of SIRT3 with plasmid, activation SIRT3 with honokiol, and supplementation with the SIRT3 cofactor nicotinamide adenine dinucleotide [NAD
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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.