Endogenous Vasoactive Peptides and Vascular Aging-Related Diseases

Figure 4

The mechanisms of CGRP in protecting against EC and VSMC injury. In ECs, CGRP improves endothelial function by increasing eNOS/NO expression, upregulating telomerase activity, and inhibiting ERK1/2-NOX4 via binding to its receptor complex CRLR/RAMP1. In VSMCs, CGRP attenuates apoptosis by inhibiting the CaMKII/CREB signaling pathway, inhibiting oxidative stress by blocking the Src/STAT3 signaling pathway, and protecting against inflammation via the EGFR-ERK1/2 pathway. Abbreviations: CGRP: calcitonin gene-related peptide; CRLR: calcitonin receptor-like receptor; RAMP: receptor activity-modifying protein; eNOS: endogenous nitric oxide synthase; NO: nitric oxide; ERK: extracellular regulated protein kinase; NOX: NADPH oxidase enzyme; CaMKII: calmodulin-dependent protein kinase II; CREB: cAMP-responsive element-binding protein; STAT3: signal transducers and activators of transduction-3; EGFR: epidermal growth factor receptor; ECs: endothelial cells; VSMCs: vascular smooth muscle cells.