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In a mouse model of pressure-overload heart failure, the inhibitor significantly alleviated myocardial remodeling and dysfunction by inhibiting H 2 S degradation, demonstrating the feasibility of targeting the H 2 S metabolic pathway for treating heart failure

First, glutamate-cysteine ligase (GCL) links glutamate and cysteine to form -glutamyl cysteine (rate-limiting steps)

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