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Titolo:
Complement activation in heart diseases: Role of oxidants
Autore:
Chakraborti, T; Mandal, A; Mandal, M; Das, S; Chakraborti, S;
Indirizzi:
Univ Kalyani, Dept Biochem & Biophys, Kalyani 741235, W Bengal, India UnivKalyani Kalyani W Bengal India 741235 alyani 741235, W Bengal, India Univ Florida, Inst Brain, Dept Neurosci, Gainesville, FL 32610 USA Univ Florida Gainesville FL USA 32610 Neurosci, Gainesville, FL 32610 USA
Titolo Testata:
CELLULAR SIGNALLING
fascicolo: 9-10, volume: 12, anno: 2000,
pagine: 607 - 617
SICI:
0898-6568(200010)12:9-10<607:CAIHDR>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; MEMBRANE ATTACK COMPLEX; RABBIT ISOLATED HEART; MYOCARDIAL-ISCHEMIA; INDEPENDENT ACTIVATION; PULMONARY ENDOTHELIUM; SELECTIVE-INHIBITION; NEUTROPHIL ADHESION; MEDIATED ACTIVATION; CARDIAC MYOCYTES;
Keywords:
oxidants; ischemia/reperfusion injury; complements; neutrophils; endothelium; myocytes; myocardial infarction; adhesion molecules; nitric oxide; soluble complement receptor 1; selectins; protectin; integrins; clusterin; membrane attack complex; C-reactive protein; heparin; mitochondria;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
84
Recensione:
Indirizzi per estratti:
Indirizzo: Chakraborti, S Univ Kalyani, Dept Biochem & Biophys, Kalyani 741235, W Bengal, India Univ Kalyani Kalyani W Bengal India 741235 W Bengal, India
Citazione:
T. Chakraborti et al., "Complement activation in heart diseases: Role of oxidants", CELL SIGNAL, 12(9-10), 2000, pp. 607-617

Abstract

Increasing evidence demonstrated that atherosclerosis is an immunologically mediated disease. Myocardial ischemia/reperfusion injury is accompanied by an inflammatory response contributing to reversible and irreversible changes in tissue viability and organ function. Three major components are recognized as the major contributing factors in reperfusion injury. These are: (1) molecular oxygen; (2) cellular blood elements (especially the neutrophils); and (3) components of the activated complement system. The latter two often act in concert. Endothelial and leukocyte responses are involved in tissue injury, orchestrated primarily by the complement cascade. Anaphylatoxins and assembly of the membrane attack complex contribute directly and indirectly to further tissue damage. Tissue damage mediated by neutrophils canbe initiated by complement fragments, notably C5a, which are potent stimulators of neutrophil superoxide production and adherence to coronary artery endothelium. The complement cascade, particularly the alternative pathway, is activated during myocardial ischemia/reperfusion. Complement fragments such as the anaphylatoxins C3a and C5a, are produced both locally and systematically, and the membrane attack complex is deposited on cell membranes and subsequent release of mediators such as histamine and platelet activatingfactor (PAF), thereby causing an increase in vascular permeability with concomitant manifestation of cellular edema. Complement increases the expression of CD18 on the neutrophils and increases P-selectin expression on the surface of the endothelium. Mitochondria may be a source of molecules that activate complements during ischemia/reperfusion injury to myocardium, providing therewith a stimulus for infiltration of polymorphonuclear leukocytes. Tissue salvage can be achieved by depletion of complement components, thusmaking evident a contributory role for the complement cascade in ischemia/reperfusion injury. The complexities of the complement cascade provide numerous sites as potential targets for therapeutic interventions designed to modulate the complement response to injury. The latter is exemplified by theability of soluble form of complement receptor 1 (sCR1) to decrease infarct size in in vitro models of ischemia/reperfusion injury. The mechanism(s) that initiates complement activation is not clearly known, although loss ofCD59 (protectin) from cells compromised by ischemia/reperfusion may contribute to direct damage of the coronary vascular bed by the terminal complement complex. Therapeutic approaches to ischemia/reperfusion injury in general, and especially those involving complements, are at the very beginning and their potential benefits have still to be adequately evaluated. It may benoted that complement activation has both positive and negative effects and, therefore, might be modulated rather than abruptly blunted. (C) 2000 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 01:03:52