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Genetic or pharmacologic loss of FABP5 disrupts mitochondrial cristae structure, resulting in release of mtDNA, and triggers cGAS-STING-dependent type I interferon signaling, which promotes Treg cell suppressive function and enhances antitumor immunity (101) (Figure 2)

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[DOI] [PubMed] [Google Scholar] 17.Pescatello LS, Arena S, Riebe D, Paul D

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While not necessarily a clinically applicable strategy, this discovery raised the intriguing possibility that with a better understanding of the molecular pathways responsible for this injury, treatments could be developed to further reduce morbidity and mortality in AMI

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177 Other conditions with similar clinical features include thyroid disease, hyperprolactinemia (high levels of the hormone prolactin), an androgen-producing tumor of the ovary or adrenal gland, and non-classical congenital adrenal hyperplasia (NC-CAH), which causes adrenal steroid 21-hydroxylase deficiency

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