Key result
Metabotropic glutamate receptor 5 blockade using MTEP ameliorated PAH-induced pathological right cardiac remodelling in rats by inhibiting PI3K/AKT, P38MAPK, Ang 2, and VEGF signalling cascades.
Why the study?
Glutaminolysis plays a crucial role in PAH-induced remodelling and mGluR5 may mediate this process, prompting investigation into whether mGluR5 blockade attenuates pathological cardiac remodelling.
Does mGluR5 blockade with MTEP attenuate pathological cardiac remodeling in a rat model of monocrotaline-induced pulmonary arterial hypertension?
Population
Male Sprague-Dawley rats with monocrotaline-induced pulmonary arterial hypertension
Comparison
MTEP (10 mg/kg intraperitoneally) vs control
Design
Animal experimental study
Authors
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MTEP effects on right ventricular remodeling remain preclinical; leaves open whether mGluR5 blockade merits human PAH trials.
Does mGluR5 blockade with MTEP attenuate pathological cardiac remodeling in a rat model of monocrotaline-induced pulmonary arterial hypertension?
Metabotropic glutamate receptor 5 blockade using MTEP ameliorates PAH-induced pathological right cardiac remodeling in a preclinical rat model.
Mprah et al. (2022) studied Pulmonary arterial hypertension. 3-((2-Methyl-4-thiazolyl)ethynyl)pyridine (MTEP) vs. MCT-induced PAH rats (control) was evaluated on Hemodynamics, right ventricular hypertrophy, and protein expressions of remodelling and inflammatory markers. Metabotropic glutamate receptor 5 blockade using MTEP ameliorated PAH-induced pathological right cardiac remodelling in rats by inhibiting PI3K/AKT, P38MAPK, Ang 2, and VEGF signalling cascades.
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