ArticleMedical science monitor basic research2016
Activation of AMPK Prevents Monocrotaline-Induced Extracellular Matrix Remodeling of Pulmonary Artery.
Article in Medical science monitor basic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Inhibiting HIF-1α-Induced miR-663b Improves Pulmonary Arterial Hypertension by Reducing Dysfunctions of PASMCs Through Repressing Sirt1-ZBP1-Mediated PANoptosis.Journal of cellular and molecular medicine · 2026Article
- Theoretical and Experimental Bacterial Adherence on Chitosan Films with Varied Characteristics.International journal of molecular sciences · 2026Article
- Monocrotaline-Induced Pulmonary Arterial Hypertension and Bosentan Treatment in Rats: Focus on Plasma and Erythrocyte Parameters.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Protective effects of metformin in various cardiovascular diseases: Clinical evidence and AMPK-dependent mechanisms.Journal of cellular and molecular medicine · 2022Review
- AMPK and the Challenge of Treating Hypoxic Pulmonary Hypertension.International journal of molecular sciences · 2022Review
- Metformin inhibits pulmonary artery smooth muscle cell proliferation by upregulating p21 via NONRATT015587.2.International journal of molecular medicine · 2022Article
- Differential Expression Profile of microRNAs and Tight Junction in the Lung Tissues of Rat With Mitomycin-C-Induced Pulmonary Veno-Occlusive Disease.Frontiers in cardiovascular medicine · 2022Article
- Effects of the peripheral CBFrontiers in pharmacology · 2022Article
- Lessons from Cancer Metabolism for Pulmonary Arterial Hypertension and Fibrosis.American journal of respiratory cell and molecular biology · 2021Review
- Zingerone Attenuates Pi-induced Vascular Calcification via AMPK-mediated TIMP4 Expression.Journal of lipid and atherosclerosis · 2021Article
- AMPK and Pulmonary Hypertension: Crossroads Between Vasoconstriction and Vascular Remodeling.Frontiers in cell and developmental biology · 2021Review
- Decreased AMP-activated protein kinase (AMPK) function and protective effect of metformin in neonatal rat pups exposed to hyperoxia lung injury.Physiological reports · 2020Article
- AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2020Article
- Lower Body Weight in Rats Under Hypobaric Hypoxia Exposure Would Lead to Reduced Right Ventricular Hypertrophy and Increased AMPK Activation.Frontiers in physiology · 2020Article
- Metformin as a protective agent against natural or chemical toxicities: a comprehensive review on drug repositioning.Journal of endocrinological investigation · 2020Review
- Metabolic reprogramming of the urea cycle pathway in experimental pulmonary arterial hypertension rats induced by monocrotaline.Respiratory research · 2018Article
- Metabolic Status in Patients with Operable vs. Inoperable Left-to-Right Shunts.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Pulmonary Arterial Stiffness: An Early and Pervasive Driver of Pulmonary Arterial Hypertension.Frontiers in medicine · 2018Review
- Metformin Suppresses Proliferation and Viability of Rat Pheochromocytoma Cells.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe current study was performed to investigate the effect of adenosine monophosphate (AMP) - activated protein kinase (AMPK) activation on the extracellular matrix (ECM) remodeling of pulmonary arteries in pulmonary arterial hypertension (PAH) and to address its potential mechanisms. MATERIAL AND
methodsPAH was induced by a single intraperitoneal injection of monocrotaline (MCT) into Sprague-Dawley rats. Metformin (MET) was administered to activate AMPK. Immunoblotting was used to determine the phosphorylation and expression of AMPK and expression of tissue inhibitor of metalloproteinase-1 (TIMP-1). Gelatin zymography was performed to determine the activity of matrix metalloproteinase-2 (MMP-2) and MMP-9.
resultsActivation of AMPK by MET significantly reduced the right ventricle systolic pressure and the right ventricular hypertrophy in MCT-induced rat PAH model, and partially inhibited the ECM remodeling of pulmonary arteries. These effects were coupled with the decrease of MMP-2/9 activity and TIMP-1 expression.
conclusionsThis study suggests that activation of AMPK benefits PAH by inhibiting ECM remodeling of pulmonary arteries. Enhancing AMPK activity might have potential value in clinical treatment of PAH.
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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.