Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion.

Buerke, Michael; Murohara, Toyoaki; Skurk, Carsten; Nuss, Charles; Tomaselli, Kevin J.; Lefer, Allan M.

doi:10.1073/pnas.92.17.8031

Cited by 370 publications

(222 citation statements)

References 32 publications

(42 reference statements)

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“…7,18,24 Thus, we reasoned that the direct injection of the adenovirus expressing constitutively active Akt could minimize myocyte apoptosis in the affected region of the heart. Furthermore, because adenovirus-mediated gene transfer permits acute delivery of recombinant protein, we reasoned that this model would provide a more direct test of protein function than transgenic animals, in which secondary effects of chronic expression can confound analyses.…”

Section: Discussionmentioning

confidence: 99%

“…7 Thus, we investigated whether expression of constitutively active Akt could protect murine myocardium from reperfusion injury ( Figure 6A). In this model, adenoviral constructs were injected directly into the apical and anterolateral free wall of the heart, a region that shows a large perfusion defect after occlusion of the left coronary artery as determined by staining with Evans blue dye ( Figure 6B).…”

Section: Constitutively Active Akt Protects Myocardium From Apoptosismentioning

confidence: 99%

“…7 More recently, it has been shown that IGF-1 functions as a cell survival factor for cultured cardiac myocytes exposed to doxorubicin in the absence of serum. 8 Therefore, analysis of the IGF-1 signaling pathways, especially with respect to cell survival, may lead to the development of clinical strategies to treat heart disease.…”

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confidence: 99%

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Akt Promotes Survival of Cardiomyocytes In Vitro and Protects Against Ischemia-Reperfusion Injury in Mouse Heart

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Section: Constitutively Active Akt Protects Myocardium From Apoptosismentioning

confidence: 99%

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Akt Promotes Survival of Cardiomyocytes In Vitro and Protects Against Ischemia-Reperfusion Injury in Mouse Heart

et al. 2000

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“…Finally, the addition of IL-6 or CNTF has relatively little effect, whereas the addition of another member of the IL-6 family (LIF), which uses an identical heterodimer pathway for activating downstream cardiac muscle cell responses via gp130 and LIF receptor ␤ (3), has a similar effect on the blockade of the apoptotic signaling pathway. Insulin-like growth factor 1, which has been shown to be cardioprotective in a murine model of myocardial ischemia reperfusion (29), could also inhibit cardiac myocyte apoptosis. Taken together, these studies provide the first evidence that cardiotrophin 1 promotes cardiac myocyte survival through the activation of pathways that can interrupt the apoptotic signaling cascade.…”

Section: Ct-1-dependent Pathways Promote Myocardial Cell Survival Viamentioning

confidence: 99%

Cardiotrophin 1 (CT-1) Inhibition of Cardiac Myocyte Apoptosis via a Mitogen-activated Protein Kinase-dependent Pathway

Sheng¹,

Knowlton

Chen³

et al. 1997

Journal of Biological Chemistry

380

212

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Cardiac muscle cell survival plays a critical role in maintaining the normal function of the heart and possibly in cardiac development. Adult cardiac muscle cells are terminally differentiated and therefore have lost their proliferative capacity. In contrast to skeletal muscle, the myocardium does not contain satellite heart muscle cells, and irreversible heart injury results in scarring and an eventual decrease in global cardiac function. In response to mechanical stimuli and hemodynamic stress, the adult myocardium activates an adaptive hypertrophic response that is characterized by an increase in myocardial cell size without a concomitant increase in myocyte number (For review, see Refs. 1 and 2). However, during longstanding exposure to hypertension or other forms of hemodynamic stress, a distinct form of myocardial cell hypertrophy can be activated in which the heart becomes dilated and individual cardiac myocytes exhibit an increase in cell length, reflecting the addition of new sarcomeric units in series (3,4). This dilatation of the heart is usually accompanied by fibrosis, microscarring, and the loss of viable cardiac myocytes throughout the myocardium. As a result of cardiac dilatation and myocyte dropout, the myocardium ultimately develops an irreversible loss of function and ensuing cardiac muscle failure (4). As such, the identification of the signaling pathways that mediate distinct forms of cardiac muscle cell hypertrophy, dysfunction, and cardiac muscle cell survival are critical to the ultimate elucidation of the molecular basis of cardiac muscle failure.By coupling expression cloning with an embryonic stem cellbased model of in vitro cardiogenesis (5), recent studies have identified cardiotrophin 1 (CT-1), 1 a novel cardiac cytokine that was isolated in a search for new factors that induce cardiac myocyte hypertrophy (5). CT-1 is a new member of the IL-6 family of cytokines that exert their biological effects through the shared signaling subunit gp130 (3, 5-7) and can activate a distinct form of myocardial cell hypertrophy that is characteristic of volume overload cardiac hypertrophy at the molecular, morphological, and cellular levels (3). Importantly, cardiotrophin 1 has been shown to be capable of promoting survival of both embryonic and neonatal rat ventricular muscle cells (8). Recent studies have demonstrated that CT-1 exerts its effects on cardiac muscle cell hypertrophy through promoting the heterodimerization of gp130 with the leukemia inhibitory factor

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“…En un modelo similar de daño isquémico miocárdico se ha demostrado que un inhibidor de las caspasas, el ZVAD-fmk, disminuye la apoptosis de los cardiomiocitos y reduce el área de infarto con respecto a los animales no tratados 57 . En roedores tratados con el factor de crecimiento similar a la insulina tipo 1, por vía sistémica 58 o mediante transfección 59 , se constató una menor aparición de apoptosis miocárdica tras la inducción del infarto que en los animales no tratados. Además, los animales que recibieron el factor presenta-ron menos remodelado de la pared ventricular y menos compromiso de la función ventricular que los animales sin tratar.…”

Section: En El áMbito De La Modulación Farmacológica De La Apoptosisunclassified

Apoptosis en las enfermedades cardiovasculares

Díez¹

2000

Revista Española de Cardiología

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INTRODUCCIÓNDesde las primeras descripciones clásicas de Virchow se reconocía un tipo de muerte celular: la necrosis. Sin embargo, a finales del siglo pasado, Walter Flemming describió un tipo de muerte celular con características morfológicas diferentes, al que denominó cromatólisis. Tuvo que transcurrir casi un siglo hasta que este tipo de muerte celular fuese adecuadamente caracterizado por Kerr, quien en 1972 propuso el tér-mino apoptosis para denominarlo 1 .En los últimos 20 años, la apoptosis y la necrosis se han considerado como los dos tipos fundamentales de muerte celular. Sin embargo, Majno y Joris han puesto de manifiesto la inconsistencia de este concepto 2 . En efecto, en términos estrictos, la necrosis representa el conjunto de cambios degradativos en los que culmina cualquier tipo de muerte celular. Así, a la necrosis se llega tanto por un proceso de apoptosis, morfológica-mente caracterizado por el arrugamiento y la fragmentación de la célula, como por un proceso de oncosis, en el que la célula se hincha y estalla. Por lo tanto, hoy día cabe distinguir dos tipos fundamentales de muerte celular: el apoptótico y el oncocítico. La apoptosis constituye una forma de muerte celular con características morfológicas y dinámicas distintas de la muerte por oncosis o por necrosis. Desde el punto de vista de la arquitectura celular, la apoptosis equilibra el efecto de la proliferación celular. Por ello, las alteraciones de la regulación de la apoptosis pueden participar en el desarrollo de numerosas enfermedades. Es el caso de la apoptosis exagerada, que conduce a la atrofia y al fallo de la función de un órgano, o de la apoptosis insuficiente, que propicia el remodelado estructural organotisular. En los últimos años se asiste a una gran expansión en la investigación sobre apoptosis, una investigación en la que también participa la comunidad cardiovascular. Desde muy diversos ámbitos de la medicina cardiovascular se han aportado observaciones sobre el posible papel de la apoptosis en síndromes que oscilan desde los defectos de conducción hasta la insuficiencia cardíaca congestiva, desde la aterosclerosis hasta los aneurismas. No hay duda de que esas observaciones puntuales acabarán configurando conceptos etiopatogénicos y fisiopatológi-cos que serán la base del diseño de nuevas estrategias diagnósticas y terapéuticas. A R T Í C U L O D E R E V I S I Ó N

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Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion.

Cited by 370 publications

References 32 publications

Akt Promotes Survival of Cardiomyocytes In Vitro and Protects Against Ischemia-Reperfusion Injury in Mouse Heart

Akt Promotes Survival of Cardiomyocytes In Vitro and Protects Against Ischemia-Reperfusion Injury in Mouse Heart

Cardiotrophin 1 (CT-1) Inhibition of Cardiac Myocyte Apoptosis via a Mitogen-activated Protein Kinase-dependent Pathway

Apoptosis en las enfermedades cardiovasculares

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