Figure 1.

Lipolysis and DNA damage promote the release of EVs by adipocytes in a p53-dependent manner. Lipolytic stimuli activate p53 and promote the release of lipid-rich AdEVs. DNA damage and pharmacologic activation of p53 suppress the activity of mTORC1, which relieves the inhibition on free protein release and the packaging and/or release of AdEVs. The resultant AdEVs contain various types of cargo, including cytosolic, nuclear, and mitochondrial proteins. Conversely, genetic deletion or inhibition of p53 leads to impaired release of AdEVs and other secreted free proteins. The mechanisms by which mTORC1 regulates p53-dependent release of adipocyte-derived proteins and EVs are not yet well defined. β₃AR, β-3 adrenergic receptor. Created with BioRender.com.