Data for: Endogenous Retinoic Acid Theory and Retinoic Acid Depletion Syndrome

Retinoic acids also manage their own metabolisms with feedback mechanisms. Despite such compensatory mechanisms, the retinoic acid stores of the body get depleted due to overuse of the RIG-I pathway and the Type-I interferon synthesis patway, which include retinoic acid receptors, because of reasons such as high fever, severe catabolic process and oversized viral genome (SARS-CoV-2). As a result, the RIG-I path is passivated, causing excessive TNFα and cytokine discharge over the NFκB arm by shifting to TLR3, TLR7, TLR8, TLR9, MDA5 and UPS pathways in the mechanism, adaptive immune defense neutrophils, macrophages and dendritic cells.

Depletion of retinoic acid stores as a result of such overuse, leading to shifting of the immune defense mechanism to the NFκB arm, where retinoic acid cannot be used and which results in cytokine release, is called ‘’retinoic acid depletion syndrom’’. COVID-19 and each of the previously defined sepsis, SIRS and ARDS are essential a retinoic acid depletion syndrome. We claim that retinoic acid metabolism is defective especially in COVID-19 (cytokine storm) most inflammatory diseases such as sepsis, SIRS and ARDS.

Finding a solution to this mechanism will require a new perspective and treatment approach to such diseases.