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\begin{document}

\title{Ferroptosis activate retinoic acid inflammation ignite the development
of Silicosis}



\author[1]{XINGJIE LI}%
\author[1]{Jinzhuo Tan}%
\author[1]{renlan wu}%
\author[1]{Zongde Zhang}%
\affil[1]{The Affiliated Hospital of Southwest Medical University}%


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  \date{May 25, 2024}


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\begin{abstract}
Lung cells damage caused by inhalation of silica and silicon crystals
leads to Silicosis. Retinoic acid is a mitogen in the development of
lung organs and exerts pleiotropic effects on immune reactions. How
retinoic acid signaling engaged in Silicosis remains unknown. We report
here that retinoic acid signaling in dendritic cells was activated in
silicosis lesions. SiO2 activates the retinoic acid signaling by
provoking ferroptosis. Ferroptosis trigger a downstream ``retinoic acid
inflammation'' characterized by upregulating cGAS-STING signaling genes
and inflammasome associated IL-1\selectlanguage{greek}β\selectlanguage{english}and IL-1\selectlanguage{greek}α. \selectlanguage{english}However, knockdown of
retinoic acid receptor \selectlanguage{greek}α \selectlanguage{english}slightly mitigates ferroptosis-induced cell
death. Inhibition of ferroptosis in mice relieves silica-induced lung
inflammation and fibrosis. This cellular retinoic acid response may act
as a cytosolic adjuvant to promote extended and upgraded inflammation.
Our work unveils a mechanism by which retinoic acid reaction integrates
cGAS-STING and inflammasome signaling to sustain silica-induced
inflammation.%
\end{abstract}%



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\verb`Ferroptosis activate retinoic acid inflammation ignite the development of Silicosis.doc`  available at \url{https://authorea.com/users/738323/articles/712680-ferroptosis-activate-retinoic-acid-inflammation-ignite-the-development-of-silicosis}

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