| First Author | Ziff OJ | Year | 2018 |
| Journal | Cardiovasc Res | Volume | 114 |
| Issue | 3 | Pages | 358-367 |
| PubMed ID | 29040423 | Mgi Jnum | J:261097 |
| Mgi Id | MGI:6151350 | Doi | 10.1093/cvr/cvx203 |
| Citation | Ziff OJ, et al. (2018) Therapeutic strategies utilizing SDF-1alpha in ischaemic cardiomyopathy. Cardiovasc Res 114(3):358-367 |
| abstractText | 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-1alpha 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-1alpha release and CXCR4 upregulation may not be optimal. Furthermore, current ELISA-based assays cannot distinguish between active SDF-1alpha, and SDF-1alpha inactivated by dipeptidyl peptidase 4 (DPP4). Current therapeutic approaches aim to recruit the SDF-1alpha-CXCR4 pathway or prolong SDF-1alpha life-time by preventing its cleavage by DPP4. This review assesses the evidence supporting these approaches and proposes SDF-1alpha as an important confounder in recent studies of DPP4 inhibitors. |
