Resistin worsens cardiac ischaemia-reperfusion injury

Rothwell, Sarah E.; Richards, A. Mark; Pemberton, Christopher J.

doi:10.1016/j.bbrc.2006.08.052

Cited by 51 publications

(45 citation statements)

References 39 publications

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“…These "in vitro" data were confirmed by functional studies showing that resistin induces proliferation and migration of human endothelial cell and promotes capillary-like tube formation [45,86,87]. As it was recently reported, this could be mediated via resistinactivated TWEAK (TNF-like weak inducer of apoptosis), and it is independent of altered nitric oxide (NO) production [86,88].…”

Section: Resistin and Atherosclerosismentioning

confidence: 56%

“…Moreover, resistin has been shown to impair glucose metabolism in mouse cardiomyocytes and to worsen cardiac ischemia-reperfusion injury in rats. This could be due to stimulated cardiac TNF-α secretion and the reperfusion release of 13 natriuretic peptides and biochemical markers of myocardial damage [14,87]. Furthermore, the abnormal formation of blood vessels also plays a role in other pathologies such as tumors, diabetic retinopathy, rheumatoid arthritis, or systemic lupus erythematosus.…”

Section: Resistin and Atherosclerosismentioning

confidence: 99%

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The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

372

297

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Section: Resistin and Atherosclerosismentioning

confidence: 56%

Section: Resistin and Atherosclerosismentioning

confidence: 99%

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Filková

Haluzı́k

Šenolt

2009

Clinical Immunology

372

297

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“…Resistin has been reported to contribute to the worsening of ischemia/reperfusion injury in isolated rat heart preparations [39] and to be associated with high risk in patients with congestive heart failure [40]. In addition, elevated resistin levels correlated with endothelial dysfunction [41] and with the development of atherosclerosis in mice and in patients with premature coronary artery disease [42].…”

Section: Discussionmentioning

confidence: 99%

Role of resistin in cardiac contractility and hypertrophy

Kim

Satoh

et al. 2008

Journal of Molecular and Cellular Cardiology

139

120

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Cardiovascular sequelae including diabetic cardiomyopathy constitute the major cause of death in diabetic patients. Although several factors may contribute to the development of this cardiomyopathy, the underlying molecular/cellular mechanisms leading to cardiac dysfunction are still partially understood. Recently, a novel paradigm for the role of the adipocytokine resistin in diabetes has emerged. Resistin has been proposed to be a link between obesity, insulin resistance and diabetes. Using microarray analysis, we have recently found that cardiomyocytes isolated from type 2 diabetic hearts express high levels of resistin. However, the function of resistin with respect to cardiac function is unknown. In this study we show that resistin is not only expressed in the heart, but also promotes cardiac hypertrophy. Adenovirus-mediated overexpression of resistin in cultured neonatal rat ventricular myocytes (NRVM) significantly increased sarcomere organization and cell size, increased protein synthesis and increased the expression of atrial natriuretic factor and β-myosin heavy chain. Overexpression of resistin in NRVM was also associated with activation of the mitogenactivated protein (MAP) kinases, ERK1/2 and p38, as well as increased Ser-636 phosphorylation of insulin receptor substrate-1 (IRS-1), indicating that IRS-1/MAPK pathway may be involved in the observed hypertrophic response. Overexpression of resistin in adult cultured cardiomyocytes significantly altered myocyte mechanics by depressing cell contractility as well as contraction and relaxation velocities. Intracellular Ca 2+ measurements showed slower Ca 2+ transients decay in resistin-transduced myocytes compared to controls, suggesting impaired cytoplasmic Ca 2+ clearing or alterations in myofilament activation. We conclude that resistin overexpression alters cardiac contractility, confers to primary cardiomyocytes all the features of the hypertrophic phenotype and promotes cardiac hypertrophy possibly via the IRS-1/MAPK pathway.

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“…Resistin function is associated with obesity, diabetes and insulin resistance. Treatment with resistin impairs glucose tolerance and insulin action, whereas loss of resistin function improves insulin resistance (9,26,27) and Resistin promotes endothelial dysfunction and I/R myocardial injury (28)(29)(30). Hyperresistinemia may contribute to the impairment of cardiac contractility and diabetic cardiac function (31).…”

Section: Discussionmentioning

confidence: 99%

Resistin-induced cardiomyocyte hypertrophy is inhibited by apelin through the inactivation of extracellular signal-regulated kinase signaling pathway in H9c2 embryonic rat cardiomyocytes

et al. 2016

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Abstract. It has been reported that resistin induces, whereas apelin inhibits cardiac hypertrophy. However, the underlying molecular mechanisms of apelin inhibiting resistin-induced cardiac hypertrophy remain unclear. The aim of the current study is to investigate the effects of apelin on resistin-induced cardiomyocyte hypertrophy and elucidate the underlying molecular mechanism. H9c2 cells were used in the present study, and cell surface area and protein synthesis were evaluated. Reverse transcription-quantitative polymerase chain reaction was performed to analyze the expression levels of hypertrophic markers, brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC). In addition, western blotting was conducted to examine phosphorylation of extracellular signal-regulated kinase (ERK)1/2. Following treatment of H9c2 cells with resistin, cell surface area, protein synthesis, and BNP and β-MHC mRNA expression levels were increased. Subsequent to co-treatment of H9c2 cells with apelin and resistin, lead to the inhibition of resistin-induced hypertrophic effects by apelin. In addition, treatment with resistin increased phosphorylation of ERK1/2, whereas pretreatment with apelin decreased phosphorylation of ERK1/2, which was increased by resistin. These results indicate that resistin-induced cardiac hypertrophy is inhibited by apelin via inactivation of ERK1/2 cell signaling.

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Resistin worsens cardiac ischaemia-reperfusion injury

Cited by 51 publications

References 39 publications

The role of resistin as a regulator of inflammation: Implications for various human pathologies

The role of resistin as a regulator of inflammation: Implications for various human pathologies

Role of resistin in cardiac contractility and hypertrophy

Resistin-induced cardiomyocyte hypertrophy is inhibited by apelin through the inactivation of extracellular signal-regulated kinase signaling pathway in H9c2 embryonic rat cardiomyocytes

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