ArticleBritish journal of pharmacology2016
Inhibition of fatty acid synthase is protective in pulmonary hypertension.
Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 69 citations in OpenAlex.
- Metabolic Markers as Potential Risk Factors in Pulmonary Hypertension.Pulmonary circulation · 2026Article
- Macrophage κ-opioid receptor inhibits hypoxic pulmonary hypertension progression and right heart dysfunction via an SCD1-dependent anti-inflammatory response.Genes & diseases · 2026Article
- Mechanisms Underlying Altitude-Induced and Group 3 Pulmonary Hypertension.International journal of molecular sciences · 2026Review
- Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026Review
- Roles of Lipid Metabolism in Pulmonary Hypertension: Friend or Foe?Biomolecules · 2025Review
- The Interplay Between Pulmonary Hypertension and Atrial Fibrillation: A Comprehensive Overview.Cells · 2025Review
- Metabolic reprogramming and interventions in angiogenesis.Journal of advanced research · 2025Review
- Ginsenoside Rg1 improves hypoxia-induced pulmonary vascular endothelial dysfunction through TXNIP/NLRP3 pathway-modulated mitophagy.Journal of ginseng research · 2025Article
- Glycolysis modulation: New therapeutic strategies to improve pulmonary hypertension (Review).International journal of molecular medicine · 2024Review
- Unveiling the metabolic landscape of pulmonary hypertension: insights from metabolomics.Respiratory research · 2024Review
- Fatty acid synthase inhibition improves hypertension-induced erectile dysfunction by suppressing oxidative stress and NLRP3 inflammasome-dependent pyroptosis through activating the Nrf2/HO-1 pathway.Frontiers in immunology · 2024Article
- Metabolic reprogramming, oxidative stress, and pulmonary hypertension.Redox biology · 2023Review
- Cardiometabolic Risk Factors Associated With Right Ventricular Function and Compensation in Patients Referred for Echocardiography.Journal of the American Heart Association · 2023Article
- E-cigarettes Induce Dysregulation of Autophagy Leading to Endothelial Dysfunction in Pulmonary Arterial Hypertension.Stem cells (Dayton, Ohio) · 2023Article
- Inhibition of fatty acid synthase protects obese mice from acute lung injury via ameliorating lung endothelial dysfunction.Respiratory research · 2023Article
- Comparative transcription profiling of mRNA and lncRNA in pulmonary arterial hypertension after C75 treatment.BMC pulmonary medicine · 2023Article
- Acquired disorders of mitochondrial metabolism and dynamics in pulmonary arterial hypertension.Frontiers in cell and developmental biology · 2023Review
- Identification of Zip8-correlated hub genes in pulmonary hypertension by informatic analysis.PeerJ · 2023Article
- Fatty Acid Metabolism in Endothelial Cell.Genes · 2022Review
- Metabolism, Mitochondrial Dysfunction, and Redox Homeostasis in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeIn pulmonary hypertension (PH), similar to cancer, there is altered energy metabolism, apoptosis resistance and cellular proliferation leading to pulmonary vascular remodelling. Proliferating cells exhibit higher rate of de novo fatty acid synthesis to provide lipids for membrane formation and energy production. As inhibition of de novo fatty acid synthesis proved protective in cancer experimentally, therefore, it was hypothesized that modulation of de novo fatty acid synthesis by inhibition of fatty acid synthase (FAS) may prove beneficial for PH. EXPERIMENTAL APPROACH: For in vitro studies, human pulmonary artery smooth muscle cells (HPASMCs) were exposed to hypoxia and to induce PH in vivo, rats were treated with monocrotaline (MCT). FAS was inhibited by siRNA (60 nM) and C75 (2 mg·kg(-1) , i.p. once a week for 5 weeks) in in vitro and in vivo studies respectively.
resultsIncreased expression and activity of FAS were observed in hypoxic HPASMCs and lungs of MCT-treated rats. Inhibition of FAS increased apoptosis and glucose oxidation, but decreased proliferation and markers of autophagy, glycolysis and insulin resistance in hypoxic HPASMCs. It also improved the mitochondrial functions as evident by increased level of ATP and restoration of normal level of ROS and membrane potential of mitochondria. In MCT-treated rats, FAS inhibition decreased right ventricular pressure, hypertrophy, pulmonary vascular remodelling (increased apoptosis and decreased proliferation of cells) and endothelial dysfunction in lungs.
conclusionsOur results demonstrate that FAS activity is modulated in PH, and its inhibition may provide a new therapeutic approach to treat PH.
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