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Its depletion can increase the toxicity of arsenic in various cell types via mechanisms including increased oxidative stress and free active arsenic concentration, loss of arsenic-bound mercaptan, and reduction in the detoxification by GSHdependent methylation and the binding of arsenic to GSH

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TGF- induces GLS1 via the PI3K/mTORC2/PDGFR signaling pathway, promoting fibrotic target expression [100]

Current research emphasizes neutrophil activation, recruitment, and NETs production, which could inform therapeutic strategies targeting neutrophils for the prevention and treatment of CVDs