Cytokines and the Microcirculation in Ischemia and Reperfusion

Frangogiannis, Nikolaos G.; Youker, Keith A.; Rossen, Roger D.; Gwechenberger, Marianne; Lindsey, Merry L.; Mendoza, Leonardo H.; Michael, Lloyd H.; Ballantyne, Christie M.; Smith, C. W.; Entman, Mark L.

doi:10.1006/jmcc.1998.0829

Cited by 169 publications

(125 citation statements)

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“…Numerous studies have demonstrated activation of cytokine cascades in the infarcted myocardium [142], [143], [144]. Induction and release of the pro-inflammatory cytokines TNF-α, IL-1β and IL-6 is consistently found in experimental models of myocardial infarction [144], [145], [11].…”

Section: Pro-inflammatory Cytokines In Myocardial Infarctionmentioning

confidence: 99%

“…Induction and release of the pro-inflammatory cytokines TNF-α, IL-1β and IL-6 is consistently found in experimental models of myocardial infarction [144], [145], [11]. Complement activation, ROS generation and NF-κB activation potently stimulate cytokine mRNA synthesis in both resident and blood-derived cells, resulting in marked cytokine upregulation in the infarcted area.…”

Section: Pro-inflammatory Cytokines In Myocardial Infarctionmentioning

confidence: 99%

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The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

568

499

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Myocardial infarction is the most common cause of cardiac injury and results in acute loss of a large number of myocardial cells. Because the heart has negligible regenerative capacity, cardiomyocyte death triggers a reparative response that ultimately results in formation of a scar and is associated with dilative remodeling of the ventricle. Cardiac injury activates innate immune mechanisms initiating an inflammatory reaction. Toll Like Receptor-mediated pathways, the complement cascade and reactive oxygen generation induce Nuclear Factor (NF)-κB activation and upregulate chemokine and cytokine synthesis in the infarcted heart. Chemokines stimulate the chemotactic recruitment of inflammatory leukocytes into the infarct, while cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. Monocyte subsets play distinct roles in phagocytosis of dead cardiomyocytes and in granulation tissue formation through the release of growth factors. Clearance of dead cells and matrix debris may be essential for resolution of inflammation and transition into the reparative phase. Transforming Growth Factor (TGF)-β plays a crucial role in cardiac repair by suppressing inflammation while promoting myofibroblast phenotypic modulation and extracellular matrix deposition. Myofibroblast proliferation and angiogenesis result in formation of highly vascularized granulation tissue. As the healing infarct matures, fibroblasts become apoptotic and a collagen-based matrix is formed, while many infarct neovessels acquire a muscular coat and uncoated vessels regress. Timely resolution of the inflammatory infiltrate and spatial containment of the inflammatory and reparative response into the infarcted area are essential for optimal infarct healing. Targeting inflammatory pathways following infarction may reduce cardiomyocyte injury and attenuate adverse remodeling. In addition, understanding the role of the immune system in cardiac repair is necessary in order to design optimal strategies for cardiac regeneration.

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Section: Pro-inflammatory Cytokines In Myocardial Infarctionmentioning

confidence: 99%

Section: Pro-inflammatory Cytokines In Myocardial Infarctionmentioning

confidence: 99%

The immune system and cardiac repair

Frangogiannis

2008

Pharmacological Research

568

499

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“…It is well known that various cytokines are involved in myocardial I/R injury [30,31]. These cytokines are produced by several types of cells, such as neutrophils, lymphocytes, macrophages, and endothelial cells, and play an important role in the pathogenesis of myocardial I/R injury.…”

Section: Myocardial I/r Injury and Cytokinesmentioning

confidence: 99%

Activation of invariant natural killer T cells by α-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice

Homma¹,

Kinugawa²,

Takahashi³

et al. 2013

Journal of Molecular and Cellular Cardiology

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“…Redução da resposta inflamatória e dos níveis de COX-2, com aumento da expressão da MyoD foram obtidos após laserterapia em lesão realizada no músculo tibial anterior 51 . Embora Moreira et al 42 tenham observado uma tendência a maior deposição de COL I no músculo gastrocnêmio lesionado cirurgicamente mediante incisão longitudinal, após 14 dias de tratamento com LBP não houve diferença entre grupos tratado com Ga-As (p=0,15) e GaAlAs (p=0,19), em relação ao grupo controle (não submetido a radiação).…”

Section: Discussionunclassified

Laserterapia Em Afecções Locomotoras: Revisão Sistemática De Estudos Experimentais

Souza

Silva

2016

Rev Bras Med Esporte

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RESUMOIntrodução: Ao longo dos anos a fisioterapia tem contribuído para o tratamento das lesões musculotendí-neas e osteoarticulares pela utilização de diversos recursos eletrotermofototerapêuticos como, por exemplo, o laser de baixa potência. Objetivo: A finalidade desse estudo foi identificar mediante revisão sistemática, o efeito da laserterapia de baixa potência em afecções do sistema locomotor de ratos, com destaque para a dose de energia e o comprimento de onda utilizado, assim como para a resposta ao tratamento. Métodos: Foram consultadas as bases de dados Medline, Lilacs, PEDro e SciELO, entre janeiro de 2005 a maio de 2013, utilizando os termos "tendinopathy", "laser therapy", "rats", "tendon", "muscle", "bone", "low-level laser therapy", assim como "tendinopatia", "laserterapia", "ratos", "tendão", "músculo", "osso" e "laser de baixa potência". Apenas foram incluídos estudos experimentais publicados nos idiomas português e inglês, que induziram lesão em tendões, músculos, ossos e/ou articulação, tratada com laserterapia, associada ou não a outros tratamentos. Resultados: Foi encontrado um total de 30 estudos experimentais nas bases de dados consultadas, dos quais 15 (50%) foram realizados em tendão, 10 (33,33%) em músculo e cinco (16,66%) em osso e/ou articulação. As doses de energia mais comumente utilizadas foram de 3 J (26,66%) e 1 J (16,66%). Já os comprimentos de onda foram de 904 nm (21,21%) e 830 nm (21,21%). Conclusão: A informação mais expressiva obtida com a terapia foi a diminuição da resposta inflamatória (36,66%) em lesões ortopédicas agudas. May 2013, using the terms "tendinopathy", "laser therapy", "rats", "tendon", "muscle", "bone", "low-level laser therapy", as well as "tendinopatia", "laserterapia", "ratos", "tendão", " músculo", "osso" and "laser de baixa potência". Only experimental studies published in Portuguese and English and that induced lesion in tendons, muscles, bones and/or joints, treated Descritores

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Cytokines and the Microcirculation in Ischemia and Reperfusion

Cited by 169 publications

References 1 publication

The immune system and cardiac repair

The immune system and cardiac repair

Activation of invariant natural killer T cells by α-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice

Laserterapia Em Afecções Locomotoras: Revisão Sistemática De Estudos Experimentais

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