Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Shibata, Rei; Izumiya, Yasuhiro; Sato, Kaori; Papanicolaou, Kyriakos N.; Kihara, Shinji; Colucci, Wilson S.; Sam, Flora; Ouchi, Noriyuki; Walsh, Kenneth

doi:10.1016/j.yjmcc.2007.03.808

Cited by 194 publications

(156 citation statements)

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“…Moreover, adiponectinknockout mice develop exacerbated LV dilatation, myocyte hypertrophy, and contractile dysfunction after myocardial infarction compared with wild-type mice. 21) Therefore, adiponectin might protect the heart from LV remodeling, although it is unclear whether or not high adiponectin levels are a compensatory mechanism.…”

Section: Discussionmentioning

confidence: 99%

Plasma Adiponectin Levels and Left Ventricular Remodeling in Hypertrophic Cardiomyopathy

et al. 2010

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SummaryAdiponectin, which is an adipose-derived protein with antiatherosclerogenic activities, has been reported to be elevated in patients with heart failure. However, there are no reports on the significance of adiponectin in patients with hypertrophic cardiomyopathy (HCM). The purpose of this study was to elucidate the clinical significance of plasma adiponectin levels in HCM patients.Clinical characteristics, echocardiographic parameters, and levels of plasma B-type natriuretic peptide (BNP) and adiponectin were evaluated in 106 HCM patients. The plasma adiponectin levels were 10.8 ± 6.3 (range, 2.7-37.3) μg/mL. Plasma adiponectin levels were positively related to age and inversely related to body mass index (BMI). Among echocardiographic parameters, % fractional shortening (r = -0.20, P = 0.03) and maximum LV wall thickness (r = -0.23, P = 0.02) were inversely related to plasma adiponectin levels. A significant correlation between plasma adiponectin levels and BNP levels was also observed (r = 0.27, P = 0.005). In multivariate analysis, BMI, % fractional shortening, and plasma BNP levels were independent predictors of plasma adiponectin levels.Plasma adiponectin levels are associated with impaired LV systolic function in HCM patients, but not with the LV outflow gradient. Together with BNP, adiponectin can be a useful biomarker for assessing disease severity in HCM patients. (Int Heart J 2010; 51: 51-55) Key words: Hypertrophic cardiomyopathy, Adiponectin, B-type natriuretic peptide, LV remodeling, Heart failure H ypertrophic cardiomyopathy (HCM), a relatively prevalent genetic cardiac disease caused by mutations in genes encoding sarcomere proteins, is clinically defined as left ventricular (LV) hypertrophy with heterogeneous clinical and morphological features in the absence of other cardiovascular diseases.1,2) The clinical and morphological features are diverse and the natural history varies from an asymptomatic and benign clinical course to sudden premature death. [3][4][5] Biomarkers are molecules that are objectively measured by laboratory techniques, which can give us useful information in patients with cardiovascular disease, including HCM. 6) Adipocytokine adiponectin is an adipose-derived protein and shows antiatherosclerogenic and insulin-sensitizing effects. The low plasma levels of adiponectin are associated with type 2 diabetes and ischemic heart disease. [7][8][9][10][11] Moreover, the novel cardiovascular effects of adiponectin have attracted considerable attention in patients with LV hypertrophy and chronic heart failure.12-16) However, the significance of adiponectin has not yet been evaluated in patients with HCM. The purpose of this study was to elucidate the significance of plasma adiponectin levels in HCM. MethodsPatients and study protocol: The study group included 106 patients with HCM diagnosed based on echocardiographic demonstration of a hypertrophied left ventricle (maximum wall thickness ≥ 15 mm) in the absence of systemic hypertension or other cardiac disease that could produc...

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Section: Discussionmentioning

confidence: 99%

Plasma Adiponectin Levels and Left Ventricular Remodeling in Hypertrophic Cardiomyopathy

et al. 2010

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“…Previous data have reported an inverse association between measures of adiposity and plasma levels of adiponectin as well as favorable effects of higher adiponectin levels on the risk of type 2 diabetes (15)(16)(17). In a mouse model of myocardial infarction, adiponectin-knockout mice showed exacerbation of left ventricular dilation, myocyte hypertrophy, and contractile dysfunction compared with wild-type mice, 4 weeks after ligation of left anterior descending artery (18). In contrast, administration of adiponectin to wild-type mice led to decreased left ventricular dilation and interstitial fibrosis, improved left ventricular function, and diminished apoptosis (18).…”

Section: Introductionmentioning

confidence: 93%

“…In a mouse model of myocardial infarction, adiponectin-knockout mice showed exacerbation of left ventricular dilation, myocyte hypertrophy, and contractile dysfunction compared with wild-type mice, 4 weeks after ligation of left anterior descending artery (18). In contrast, administration of adiponectin to wild-type mice led to decreased left ventricular dilation and interstitial fibrosis, improved left ventricular function, and diminished apoptosis (18). Other experiments showed that adiponectin inhibits cardiac hypertrophic response to alphaadrenergic receptor stimulation (19).…”

Section: Introductionmentioning

confidence: 98%

Association Between Adiponectin and Heart Failure Risk in the Physicians' Health Study

Djoussé¹,

Wilk²,

Hanson³

et al. 2012

Obesity

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Limited data are available on the association between adiponectin and incident heart failure. In the current ancillary study to the Physicians' Health Study, we used a prospective nested-case control design to examine whether plasma adiponectin concentration was related to the risk of heart failure. We selected 787 incident heart failure cases and 787 matched controls for the current analysis. Each control was selected using a risk set sampling technique at the time of the occurrence of the index case and matched on year of birth, age at blood collection, and race. Adiponectin was measured using ELISA. Heart failure occurrence was self-reported in annual follow-up questionnaire. Validation of self-reported heart failure in this cohort has been published. The mean age was 58.7 years. In a conditional logistic regression adjusting for age, race, time of blood collection, year of birth, hypertension, atrial fibrillation, smoking, alcohol intake, and exercise, estimates of the relative risk (95% confidence interval) were 1.0 (ref), 0.74 (0.53-1.04), 0.67 (0.48-0.94), 0.70 (0.50-0.99), and 0.92 (0.65-1.30) from the lowest to the highest quintile of adiponectin, respectively, p for quadratic trend 0.004. Additional adjustment for potential mediating factors including diabetes, C-reactive protein, and body mass index led to the attenuation of the estimate of effect [1.0 (ref), 0.81 (0.57-1.15), 0.75 (0.53-1.06), 0.83 (0.58-1.18), and 1.26 (0.87-1.81) across consecutive quintiles of adiponectin]. Our data are consistent with a J-shaped association between total adiponectin and the risk of heart failure among US male physicians.Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms (18). Other experiments showed that adiponectin inhibits cardiac hypertrophic response to alphaadrenergic receptor stimulation(19). These data suggest that adiponectin may play a role in the development of HF. However, limited studies have tested such a hypothesis in a community setting among humans. Results from two previous prospective studies from Framingham and Sweden showed no statistically significant association between plasma adiponectin and incident HF. Whether these reported null findings from the above studies were due to limited statistical power in each study or absence of a causal association between adiponectin and HF risk remains unclear. Therefore, the current project sought to assess the association between total plasma adiponectin and incident HF in a prospective nested case-control study of US male physicians. Disclosures: None HHS Public Access Methods Study populationThis is an ancillary study of the Physicians' Health Study I, which is a completed randomized, double blind, placebo-controlled trial designed to study low-dose aspirin and beta-carotene for the primary prevention of cardiovascular disease and cancer. A detailed ...

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“…The sections were washed in distilled water and then stained with phosphomolybdic for 5 min, in aniline blue solution for 5 min, and then differentiated for 60 s. After a final wash in distilled water, the sections were dehydrated through 95% and 100% alcohol. Moreover, the heart tissue sections were digitally imaged in high-pixel resolution according to the method previously described (Shibata et al, 2007).…”

Section: Assessment Of Cardiac Fibrosis With Masson's Trichrome Stainingmentioning

confidence: 99%

Oral sophocarpine protects rat heart against pressure overload-induced cardiac fibrosis

Zhao

Chu

et al. 2014

Pharmaceutical Biology

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Context: Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides Linn. (Kudouzi). Sophocarpine injection was found to have significant antiviral effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in the clinic. Objective: This study assessed the effects of sophocapine on overload-induced cardiac fibrosis and investigated potential mechanisms. Materials and methods: Adult male Sprague-Dawley rats were subjected to a suprarenal abdominal aorta constriction (AC) or sham to induce sustained pressure overload. Six weeks later, rats were randomly assigned to receive sophocapine (10, 20, and 40 mg/kg, gavage) or vehicle treatment for an additional 6 weeks. Six weeks after treatment, cardiac dysfunction, cardiac coefficient, cardiac fibrosis, hydroxyproline concentration, and inflammation mediators were examined. Results: When compared with the model group, the left ventricular weight/body weight decreased by 25.4% and 39.0% in 20 and 40 mg/kg sophocarpine groups, respectively. The beneficial effects were associated with amelioration of left ventricular systolic pressure (LVSP) and left ventricular enddiastolic pressure (LVEDP). Moreover, pressure overload-induced cardiac fibrosis was attenuated in sophocarpine treated groups. Importantly, sophocarpine (20 and 40 mg/kg) decreased pro-inflammatory cytokine levels (IL-6, 14.6% and 18.5%; IL-1b, 23.1% and 32.6%), collagen content (27.7% and 50.1%), as well as matrix metalloproteinases-2, 9 (MMP-2, 9) expression (MMP-2, 11.8% and 18.5%; MMP-9, 16.2% and 21.1%). Sophocarpine (40 mg/kg) inhibited IkB-a phosphorylation (19.0%). Conclusion: These findings indicated that sophocarpine potentially had antifibrotic effects. The mechanism might be due to modulation of the balance between pro-inflammatory cytokine expression and collagen content level as well as MMPs expression via the NF-kB signaling pathway.

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Adiponectin protects against the development of systolic dysfunction following myocardial infarction

Cited by 194 publications

References 47 publications

Plasma Adiponectin Levels and Left Ventricular Remodeling in Hypertrophic Cardiomyopathy

Plasma Adiponectin Levels and Left Ventricular Remodeling in Hypertrophic Cardiomyopathy

Association Between Adiponectin and Heart Failure Risk in the Physicians' Health Study

Oral sophocarpine protects rat heart against pressure overload-induced cardiac fibrosis

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