title: The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.
abstract: Intercellular communication depends on many factors, including proteins released via the classical or non-classical secretory pathways, many of which must be properly folded to be functional. Owing to their adverse effects on the secretion machinery, stresses such as ischemia can impair the folding of secreted proteins. Paradoxically, cells rely on secreted proteins to mount a response designed to resist stress-induced damage. This review examines this paradox using proteins secreted from the heart, cardiokines, as examples, and focuses on how the ischemic heart maintains or even increases the release of select cardiokines that regulate important cellular processes in the heart, including excitation-contraction coupling, hypertrophic growth, myocardial remodeling and stem cell function, in ways that moderate ischemic damage and enhance cardiac repair.
authors.affiliation: SDSU Heart Institute and the Department of Biology, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182, USA.
authors.forename: Shirin
authors.initials: S
authors.lastname: Doroudgar
authors.forename: Christopher C
authors.initials: CC
authors.lastname: Glembotski
mesh_terms: D000818:Animals; D002450:Cell Communication; D002478:Cells, Cultured; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D007511:Ischemia / Q000473:pathology*; D009124:Muscle Proteins / Q000378:metabolism; D009206:Myocardium / Q000473:pathology*; D017510:Protein Folding; D055571:Secretory Pathway
chemical_list: D006360:Heat-Shock Proteins; D009124:Muscle Proteins