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- W2763338404 abstract "Heart failure is rapidly increasing in prevalence and will redraw the global landscape for cardiovascular health. Alleviating and repairing cardiac injury associated with myocardial infarction (MI) is key to improving this burden. Homing signals mobilize and recruit stem cells to the ischaemic myocardium where they exert beneficial paracrine effects. The chemoattractant cytokine SDF-1α and its associated receptor CXCR4 are upregulated after MI and appear to be important in this context. Activation of CXCR4 promotes both cardiomyocyte survival and stem cell migration towards the infarcted myocardium. These effects have beneficial effects on infarct size, and left ventricular remodelling and function. However, the timing of endogenous SDF-1α release and CXCR4 upregulation may not be optimal. Furthermore, current ELISA-based assays cannot distinguish between active SDF-1α, and SDF-1α inactivated by dipeptidyl peptidase 4 (DPP4). Current therapeutic approaches aim to recruit the SDF-1α-CXCR4 pathway or prolong SDF-1α life-time by preventing its cleavage by DPP4. This review assesses the evidence supporting these approaches and proposes SDF-1α as an important confounder in recent studies of DPP4 inhibitors." @default.
- W2763338404 created "2017-10-20" @default.
- W2763338404 creator A5003066373 @default.
- W2763338404 creator A5010243430 @default.
- W2763338404 creator A5057259788 @default.
- W2763338404 creator A5090808868 @default.
- W2763338404 date "2017-10-13" @default.
- W2763338404 modified "2023-09-30" @default.
- W2763338404 title "Therapeutic strategies utilizing SDF-1α in ischaemic cardiomyopathy" @default.
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- W2763338404 doi "https://doi.org/10.1093/cvr/cvx203" @default.
- W2763338404 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6005112" @default.
- W2763338404 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29040423" @default.
- W2763338404 hasPublicationYear "2017" @default.
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