title: Trans-system mechanisms against ischemic myocardial injury.
abstract: A mammalian organism possesses a hierarchy of naturally evolved protective mechanisms against ischemic myocardial injury at the molecular, cellular, and organ levels. These mechanisms comprise regional protective processes, including upregulation and secretion of paracrine cell-survival factors, inflammation, angiogenesis, fibrosis, and resident stem cell-based cardiomyocyte regeneration. There are also interactive protective processes between the injured heart, circulation, and selected remote organs, defined as trans-system protective mechanisms, including upregulation and secretion of endocrine cell-survival factors from the liver and adipose tissue as well as mobilization of bone marrow, splenic, and hepatic cells to the injury site to mediate myocardial protection and repair. The injured heart and activated remote organs exploit molecular and cellular processes, including signal transduction, gene expression, cell proliferation, differentiation, migration, mobilization, and/or extracellular matrix production, to establish protective mechanisms. Both regional and trans-system cardioprotective mechanisms are mediated by paracrine and endocrine messengers and act in coordination and synergy to maximize the protective effect, minimize myocardial infarction, and improve myocardial function, ensuring the survival and timely repair of the injured heart. The concept of the trans-system protective mechanisms may be generalized to other organ systems-injury in one organ may initiate regional as well as trans-system protective responses, thereby minimizing injury and ensuring the survival of the entire organism. Selected trans-system processes may serve as core protective mechanisms that can be exploited by selected organs in injury. These naturally evolved protective mechanisms are the foundation for developing protective strategies for myocardial infarction and injury-induced disorders in other organ systems.
authors.affiliation: Biomedical Engineering Department, Northwestern University, Evanston, Illinois Department of Emergency Medicine, Thomas Jefferson University Hospitals, Philadelphia, Pennsylvania Feinberg Cardiovascular Research Institute, Northwestern University Feinberg School of Medicine, Chicago, Illinois Carbohydrate and Lipid Metabolism Research Laboratory, College of Life Science and Technology, Dalian University, Dalian, China Department of Medicine, Division of Biological Sciences, The University of Chicago, Chicago, Illinois.
authors.forename: Shu Q
authors.initials: SQ
authors.lastname: Liu
authors.forename: Xin-Liang
authors.initials: XL
authors.lastname: Ma
authors.forename: Gangjian
authors.initials: G
authors.lastname: Qin
authors.forename: Qingping
authors.initials: Q
authors.lastname: Liu
authors.forename: Yan-Chun
authors.initials: YC
authors.lastname: Li
authors.forename: Yu H
authors.initials: YH
authors.lastname: Wu
mesh_terms: D000818:Animals; D016207:Cytokines / Q000502:physiology; D019610:Cytoprotection / Q000502:physiology; D004703:Endocrine System / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015398:Signal Transduction / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha