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CM-specific overexpression of placental growth factor (PlGF) stimulates myocardial angiogenesis and increases endothelial release of NO, resulting in myocardial hypertrophy via degradation of RGS4, a regulator of G-protein signaling involved in the CM hypertrophic response ( Animal models have also been critical in confirming mechanistic drivers of CMD in the context of comorbid metabolic derangements (Sorop et al., 2020)

Furtherly, the hepatotoxic effect of MPs has been related to activation of pyroptotic pathway, activation of NLRP3 inflammasomes and apoptosis associated speck-like protein (ASC) and increased lipid peroxidation, accompanied by ferroptosis trigger [83]

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While CNS drugs like sertraline (SRT) have shown promise in animal models, where their combination with front-line anti-TB drugs, improved early bactericidal activity, resolution of pulmonary pathology, and enhanced survival in mice infected with M.tb [70], clinical studies have raised concerns

Such an inflammation has the ability to significantly alter the gut bacteria composition and also their function