Highlights d PPARg S112 phosphorylation is crucial for its K107 SUMOylation and IL-10 suppression d PIAS2 is the specific E3 SUMOligase causing CL-mediated PPARg K107 SUMOylation d JNK-MAPK is responsible for CL-mediated PPARg S112 phosphorylation d Repurposing a clinically used JNK inhibitor can improve survival in pneumonia
In accordance with the endosymbiotic theory, mitochondrial components bear characteristic prokaryotic signatures, which act as immunomodulatory molecules when released into the extramitochondrial compartment. These endogenous immune triggers, called mitochondrial damage‐associated molecular patterns (mtDAMPs), have been implicated in the pathogenesis of various diseases, yet their role remains largely unexplored. In this review, we summarise the available literature on mtDAMPs in diseases, with a special focus on respiratory diseases. We highlight the need to bolster mtDAMP research using a multipronged approach, to study their effect on specific cell types, receptors and machinery in pathologies. We emphasise the lacunae in the current understanding of mtDAMPs, particularly in their cellular release and the chemical modifications they undergo. Finally, we conclude by proposing additional effects of mtDAMPs in diseases, specifically their role in modulating the immune system.
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