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MIF Promotes Phenotypic Switching of VSMCs via AKT / mTOR ‐Mediated Autophagy Regulation in Aortic Dissection
MIF may cause blood vessel muscle cells to change by controlling cell recycling through the AKT/mTOR pathway in aortic dissection
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Abstract
MIF was markedly upregulated in aortic dissection tissues, especially in vascular smooth muscle cells.
- MIF deficiency or treatment with ISO-1 significantly reduced the incidence, rupture, and dilation associated with aortic dissection.
- Overexpression of MIF aggravated disease progression.
- MIF may suppress autophagy by activating AKT/mTOR signaling and promoting a synthetic vascular smooth muscle cell phenotype.
- Restoration of autophagy with rapamycin reversed the phenotypic changes induced by MIF.
- Chloroquine treatment exacerbated aortic dissection.
- MIF-driven signaling may be mediated by receptors CD74 and CXCR2.
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