Does extracellular heat shock protein 70 induce cardiomyocyte inflammation and contractile dysfunction via TLR2?
Extracellular HSP70 acting via TLR2 and its obligate downstream adaptor molecule, MyD88, activate NFκB. This causes cardiomyocyte inflammation and decreased contractility.
Whole-field digital microscopy offers a means of rapidly carrying out objective, fully quantitative, and reproducible measurements of microscopic features of SSc microvascular change. The universal morphologically abnormal endothelial cells and interstitial edema in all patients with SSc biopsied suggests that SSc may be intrinsically a disease of the endothelium characterized by vascular leak.