ArticleExperimental and therapeutic medicine2020
Metformin prevents the development of monocrotaline-induced pulmonary hypertension by decreasing serum levels of big endothelin-1.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 17 citations in OpenAlex.
- Effects of sildenafil and metformin on endothelin-1 in the progression of pulmonary hypertension.Open veterinary journal · 2025Article
- Progression of pulmonary arterial hypertension: A study in model.Open veterinary journal · 2024Article
- Article
- The Correlation between Lung Ultrasound and Pathology in Rat Model of Monocrotaline-Induced Pulmonary Hypertension.Canadian respiratory journal · 2024Article
- Current Management and Future Directions for Pulmonary Arterial Hypertension Associated with Congenital Heart Disease.Journal of personalized medicine · 2023Review
- Buspirone Induces Weight Loss and Normalization of Blood Pressure via the Stimulation of PPARPPAR research · 2023Article
- Role of endothelial dysfunction in the severity of COVID‑19 infection (Review).Molecular medicine reports · 2022Review
- Article
- 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
- AMPK and Pulmonary Hypertension: Crossroads Between Vasoconstriction and Vascular Remodeling.Frontiers in cell and developmental biology · 2021Review
- The role and mechanism of AMPK in pulmonary hypertension.Therapeutic advances in respiratory diseaseReview
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Pulmonary hypertension (PH) is a disease with poor prognosis, and it is characterized by the progressive elevation of pulmonary vascular resistance and pressure. Various factors are associated with the pathology of PH, including AMP-activated protein kinase (AMPK) deficiency. The present study aimed to evaluate the therapeutic effect of metformin, an AMPK activator, in a monocrotaline (MCT)-induced PH rat model. Rats were randomly divided into the following three groups: i) Saline-injected group (sham group); ii) monocrotaline (MCT)-injected group (PH group); iii) MCT-injected and metformin-treated group (MT group). Four weeks following MCT injection, cardiac ultrasonography, invasive hemodynamic measurements, measurement of serum levels of big endothelin-1 (big ET-1) and histological analysis were performed to evaluate the effect of metformin treatment in PH. Pulmonary arterial pressure and serum big ET-1 concentrations were reduced in the MT group compared with the PH group. Medial wall thickness and wall area of the pulmonary arterioles in the MT group were decreased compared with the PH group. Comparing the right heart functional parameters among groups revealed that the acceleration time/ejection time ratio improved in the MT group compared with the PH group. Thus, the present study demonstrated the efficacy of metformin in an MCT-induced PH rat model and suggested that metformin may be a valuable, potential novel therapeutic for the treatment of PH.
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