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Damage-associated molecular patterns, such as high mobility group box 1 (HMGB1), initiate this phenotypic shift by engaging signaling pathways like toll-like receptor 4 (TLR4) and the receptor for advanced glycation end products (RAGE), which in turn activate downstream effectors, including nuclear factor kappa-B (NF-B) and the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome (Tastan and Heneka, 2024

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An original discovery: selenium deficiency and Keshan disease (an endemic heart disease)

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