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MIF purpose and signaling. MIF fulfills its Organic functions via membrane receptors and through binding to intracellular molecules. MIF’s binding to membrane receptor CD74 recruits CD44 and brings about activation of Src/MAPK signaling. MIF by way of CXCR2/4 activates PI3K/Akt downstream signaling and induces cell migration. Sustained activation of ERK1/2 phosphorylation is mediated by JUN activation domain binding protein-one (JAB1) and causes cytoplasmic phospholipase A2 (cPLA2) action (blocked by glucocorticoids) and further to arachidonate/prostaglandin generation. MIF generation may be stimulated by means of TLRs by e.g., LPS stimulation.
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more review also uncovered that MIF promotes cystic epithelial cell proliferation by activating ERK, mTOR, and Rb/E2F pathways, and regulates cystic renal epithelial cell apoptosis through p53-dependent signaling [seventy four]. Functionally, MIF deletion or blockade can hold off the cyst growth in ADPKD mice [75], indicating that MIF might contain while in the pathogenesis of ADPKD.
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with each other, MIF can be a proinflammatory cytokine and worry molecule which performs a job in immunologically and non-immunologically mediated kidney ailments like AKI and CKD. MIF is fast launched within the wounded kidney in reaction on the stimulations less than many disease circumstances. at the time introduced, MIF can activate the downstream signaling pathways which includes ERK/p38/JNK MAPK, PI3/AKT, and NF-κB signaling by way of receptors of CD74, CD44, and CXCR2/4/7, resulting in the upregulation of proinflammatory cytokines/chemokines/adhesion molecules plus the recruitment and activation of macrophages and T cells to cause progressive AKI and CKD.
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