Post-infarct remodelling: contribution of wound healing and inflammation

被引：253

作者：

Frantz, Stefan ^{[1
]}

Bauersachs, Johann ^{[1
]}

Ertl, Georg ^{[1
]}

机构：

[1] Univ Klinikum Wurzburg, Med Klin & Poliklin 1, D-97080 Wurzburg, Germany

来源：

CARDIOVASCULAR RESEARCH | 2009年 / 81卷 / 03期

关键词：

FACTOR-KAPPA-B; ACUTE MYOCARDIAL-INFARCTION; GROWTH-FACTOR-BETA; NECROSIS-FACTOR-ALPHA; LEFT-VENTRICULAR DYSFUNCTION; ANTI-C5 COMPLEMENT ANTIBODY; HEART-FAILURE; REPERFUSION INJURY; OXIDATIVE STRESS; EXTRACELLULAR-MATRIX;

D O I：

10.1093/cvr/cvn292

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and function. MI and the consequent loss of myocardium are the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains poor in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to improve healing of the cardiac wound to maintain structure and function of the heart. Healing in the heart occurs in overlapping phases. Herein, we review the inflammatory phase as a trigger of tissue formation.

引用

页码：474 / 481

页数：8

共 86 条

[1]

Pathogen recognition and innate immunity [J].

Akira, S ;

Uematsu, S ;

Takeuchi, O .

CELL, 2006, 124 (04) :783-801

[2]

Aging is associated with reduced deposition of specific extracellular matrix components, upregulation of angiogenesis, and an altered inflammatory response in a murine incisional wound healing model [J].

Ashcroft, GS ;

Horan, MA ;

Ferguson, MWJ .

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1997, 108 (04) :430-437

[3]

Increased toll-like receptor 4 in the myocardium of patients requiring left ventricular assist devices [J].

Birks, EJ ;

Felkin, LE ;

Banner, NR ;

Khaghani, A ;

Barton, PJR ;

Yacoub, MH .

JOURNAL OF HEART AND LUNG TRANSPLANTATION, 2004, 23 (02) :228-235

[4]

BORDER WA, 1994, NEW ENGL J MED, V331, P1286

[5]

Inhibition of interleukin-8 blocks myocardial ischemia-reperfusion injury [J].

Boyle, EM ;

Kovacich, JC ;

Hèbert, CA ;

Canty, TG ;

Chi, E ;

Morgan, EN ;

Pohlman, TH ;

Verrier, ED .

JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1998, 116 (01) :114-120

[6]

Pathophysiologically relevant concentrations of tumor necrosis factor-α promote progressive left ventricular dysfunction and remodeling in rats [J].

Bozkurt, B ;

Kribbs, SB ;

Clubb, FJ ;

Michael, LH ;

Didenko, VV ;

Hornsby, PJ ;

Seta, Y ;

Oral, H ;

Spinale, FG ;

Mann, DL .

CIRCULATION, 1998, 97 (14) :1382-1391

[7]

NEUTROPHILS CONTRIBUTE TO TNF INDUCED MYOCARDIAL TOLERANCE TO ISCHEMIA [J].

BROWN, JM ;

ANDERSON, BO ;

REPINE, JE ;

SHANLEY, PF ;

WHITE, CW ;

GROSSO, MA ;

BANERJEE, A ;

BENSARD, DD ;

HARKEN, AH .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1992, 24 (05) :485-495

[8]

INTERLEUKIN-1 PRETREATMENT DECREASES ISCHEMIA REPERFUSION INJURY [J].

BROWN, JM ;

WHITE, CW ;

TERADA, LS ;

GROSSO, MA ;

SHANLEY, PF ;

MULVIN, DW ;

BANERJEE, A ;

WHITMAN, GJR ;

HARKEN, AH ;

REPINE, JE .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1990, 87 (13) :5026-5030

[9]

Cardiac-specific blockade of NF-κB in cardiac pathophysiology:: differences between acute and chronic stimuli in vivo [J].

Brown, M ;

McGuinness, M ;

Wright, T ;

Ren, XP ;

Wang, Y ;

Boivin, GP ;

Hahn, H ;

Feldman, AM ;

Jones, WK .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 289 (01) :H466-H476

[10]

Cardiac failure in transgenic mice with myocardial expression of tumor necrosis factor-α [J].

Bryant, D ;

Becker, L ;

Richardson, J ;

Shelton, J ;

Franco, F ;

Peshock, R ;

Thompson, M ;

Giroir, B .

CIRCULATION, 1998, 97 (14) :1375-1381

← 1 2 3 4 5 6 7 8 9 →