Key result
Inhibition of glutaminase 1 with BPTES significantly attenuated Angiotensin II-induced cardiac hypertrophy and fibrosis in mouse models and cultured cardiac cells.
Why the study?
Does GLS1 inhibition reduce Angiotensin II-induced pathological cardiac remodeling in preclinical models?
Does GLS1 inhibition reduce Angiotensin II-induced pathological cardiac remodeling in preclinical models?
Inhibition of glutaminase 1-mediated glutaminolysis attenuates Angiotensin II-induced pathological cardiac remodeling by reducing the synthesis of aspartate and citrate necessary for cellular growth.
GLS1 inhibition merits testing in additional models; leaves open its role in treating human hypertensive heart disease.
To our knowledge, this study is the first to demonstrate that increased GLS1 expression and subsequent activation of glutaminolysis are associated with exacerbation of cardiac hypertrophy and fibrosis. Inhibiting GLS1 antagonized the adverse cardiac remodeling in vitro and in vivo, partly due to reduction of glutamine-derived metabolites, which are necessary for cellular growth and proliferation. Increased glutamine utilization for anabolic reactions in cardiac cells may be related to the pathogenesis and development of HF.
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Yoshikawa et al. (2022) studied Pathological cardiac remodeling. BPTES (Glutaminase 1 inhibitor) vs. DMSO was evaluated on Cardiac hypertrophy (heart weight to body weight ratio) and fibrosis. Inhibition of glutaminase 1 with BPTES significantly attenuated Angiotensin II-induced cardiac hypertrophy and fibrosis in mouse models and cultured cardiac cells.
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