ArticleOxidative medicine and cellular longevity2020
Combination of Dichloroacetate and Atorvastatin Regulates Excessive Proliferation and Oxidative Stress in Pulmonary Arterial Hypertension Development via p38 Signaling.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 22 citations in OpenAlex.
- Pulmonary arterial hypertension from a translational perspective: Bridging pathophysiology and treatment.Chinese medical journal · 2026Review
- Endoplasmic reticulum stress and the unfolded protein response in lung diseases: molecular pathways and therapeutic interventions.The Journal of pathology · 2026Review
- Clinical Updates in Pulmonary Hypertension.Reviews in cardiovascular medicine · 2026Review
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Dysregulation of Mitochondrial in Pulmonary Hypertension-Related Right Ventricular Remodeling: Pathophysiological Features and Targeting Drugs.Reviews in cardiovascular medicine · 2025Review
- Multidimensional study on mitochondrial dysfunction in pulmonary hypertension.Frontiers in medicine · 2025Review
- Lipid-Lowering Drugs and Pulmonary Vascular Disease: A Mendelian Randomization Study.Pulmonary circulation · 2025Article
- Oroxylin A, a broad‑spectrum anticancer agent, relieves monocrotaline‑induced pulmonary arterial hypertension by inhibiting the Warburg effect in rats.Molecular medicine reports · 2024Article
- Emerging connectivity of programmed cell death pathways and pulmonary vascular remodelling during pulmonary hypertension.Journal of cellular and molecular medicine · 2024Review
- Management of ulcerative colitis by dichloroacetate: Impact on NFATC1/NLRP3/IL1B signaling based on bioinformatics analysis combined with in vivo experimental verification.Inflammopharmacology · 2024Article
- Efficacy of atorvastatin calcium on clinical manifestations and serum inflammatory markers in elderly patients with hypertension.American journal of translational research · 2024Article
- Targeting Mitochondrial Metabolic Dysfunction in Pulmonary Hypertension: Toward New Therapeutic Approaches?International journal of molecular sciences · 2023Review
- Effect of hepatocyte growth factor on mice with hypoxic pulmonary arterial hypertension: a preliminary study.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Article
- Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension.Molecules (Basel, Switzerland) · 2022Review
- Mitochondrial dysfunction in pulmonary arterial hypertension.Frontiers in physiology · 2022Review
- Dan-Shen-Yin Granules Prevent Hypoxia-Induced Pulmonary HypertensionFrontiers in pharmacology · 2022Article
- Silencing TUFM Inhibits Development of Monocrotaline-Induced Pulmonary Hypertension by Regulating Mitochondrial Autophagy via AMPK/mTOR Signal Pathway.Oxidative medicine and cellular longevity · 2022Article
- Deletion of classical transient receptor potential 1, 3 and 6 alters pulmonary vasoconstriction in chronic hypoxia-induced pulmonary hypertension in mice.Frontiers in physiology · 2022Article
- Fasudil Dichloroacetate Alleviates SU5416/Hypoxia-Induced Pulmonary Arterial Hypertension by Ameliorating Dysfunction of Pulmonary Arterial Smooth Muscle Cells.Drug design, development and therapy · 2021Article
- Donepezil Ameliorates Pulmonary Arterial Hypertension by Inhibiting M2-Macrophage Activation.Frontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a lethal disease generally characterized by pulmonary artery remodeling. Mitochondrial metabolic disorders have been implicated as a critical regulator of excessively proliferative- and apoptosis-resistant phenotypes in pulmonary artery smooth muscle cells (PASMCs). Dichloroacetate (DCA) is an emerging drug that targets aerobic glycolysis in tumor cells. Atorvastatin (ATO) is widely used for hyperlipemia in various cardiovascular diseases. Considering that DCA and ATO regulate glucose and lipid metabolism, respectively, we hypothesized that the combination of DCA and ATO could be a potential treatment for PAH. A notable decrease in the right ventricular systolic pressure accompanied by reduced right heart hypertrophy was observed in the DCA/ATO combination treatment group compared with the monocrotaline treatment group. The DCA/ATO combination treatment alleviated vascular remodeling, thereby suppressing excessive PASMC proliferation and macrophage infiltration. In vitro, both DCA and ATO alone reduced PASMC viability by upregulating oxidative stress and lowering mitochondrial membrane potential. Surprisingly, when combined, DCA/ATO was able to decrease the levels of reactive oxygen species and cell apoptosis without compromising PASMC proliferation. Furthermore, suppression of the p38 pathway through the specific inhibitor SB203580 attenuated cell death and oxidative stress at a level consistent with that of DCA/ATO combination treatment. These observations suggested a complementary effect of DCA and ATO on rescuing PASMCs from a PAH phenotype through p38 activation via the regulation of mitochondrial-related cell death and oxidative stress. DCA in combination with ATO may represent a novel therapeutic strategy for PAH treatment.
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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 Socratic graph.