Inotropic and lusitropic, but not arrhythmogenic, effects of adipocytokine resistin on human atrial myocardium

Aitken‐Buck, Hamish M.; Babakr, Aram A; Fomison-Nurse, I.; Hout, Isabelle van; Davis, Philip J.; Bunton, Richard; Williams, Michael J.A.; Coffey, Sean; Jones, Peter P.; Lamberts, Regis R.

doi:10.1152/ajpendo.00202.2020

Cited by 4 publications

(2 citation statements)

References 38 publications

(80 reference statements)

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“…Several potential resistin receptors have been suggested but its specific one has not yet been identified and scarce information concerning the downstream signaling mechanisms of action is available (Badoer, 2021). Nevertheless, the hormone has been reported to be involved in a broad range of physiological and pathological conditions, both in rodents and in humans, acting centrally and peripherally (Aitken-Buck et al, 2020;Recinella et al, 2020;Deb et al, 2021;Rachwalik et al, 2021). In particular, resistin acting at the hypothalamic level influences energy homeostasis and modulates feeding, displaying anorexigenic effects in rodents (Brunetti et al, 2004;Tovar et al, 2005;Vázquez et al, 2008;Cifani et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Evidence that resistin acts on the mechanical responses of the mouse gastric fundus

et al. 2022

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Resistin, among its several actions, has been reported to exert central anorexigenic effects in rodents. Some adipokines which centrally modulate food intake have also been reported to affect the activity of gastric smooth muscle, whose motor responses represent a source of peripheral signals implicated in the control of the hunger-satiety cycle through the gut-brain axis. On this basis, in the present experiments, we investigated whether resistin too could affect the mechanical responses in the mouse longitudinal gastric fundal strips. Electrical field stimulation (EFS) elicited tetrodotoxin- and atropine-sensitive contractile responses. Resistin reduced the amplitude of the EFS-induced contractile responses. This effect was no longer detected in the presence of L-NNA, a nitric oxide (NO) synthesis inhibitor. Resistin did not influence the direct muscular response to methacholine. In the presence of carbachol and guanethidine, EFS elicited inhibitory responses whose amplitude was increased by resistin. L-NNA abolished the inhibitory responses evoked by EFS, indicating their nitrergic nature. In the presence of L-NNA, resistin did not have any effect on the EFS-evoked inhibitory responses. Western blot and immunofluorescence analysis revealed a significant increase in neuronal nitric oxide synthase (nNOS) expression in neurons of the myenteric plexus following resistin exposure. In conclusion, the present results offer the first evidence that resistin acts on the gastric fundus, likely through a modulatory action on the nitrergic neurotransmission.

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Section: Introductionmentioning

confidence: 99%

Evidence that resistin acts on the mechanical responses of the mouse gastric fundus

et al. 2022

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“…Numerous studies have demonstrated that resistin participates in insulin resistance, diabetes, and CVD [ 6 , 13 , 14 ]. In patients with peripheral artery disease (PAD), a higher level of resistin was associated with worsened endothelial function and an increased risk of major adverse cardiac events [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

Antiresistin Neutralizing Antibody Alleviates Doxorubicin-Induced Cardiac Injury in Mice

Wang

et al. 2022

Disease Markers

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Background. Resistin is closely related to cardiovascular diseases, and this study is aimed at examining the role of resistin in doxorubicin- (DOX-) induced cardiac injury. Methods. First, 48 mice were divided into 2 groups and treated with saline or DOX, and the expression of resistin at different time points was examined ( N = 24 ). A total of 40 mice were pretreated with the antiresistin neutralizing antibody (nAb) or isotype IgG for 1 hour and further administered DOX or saline for 5 days. The mice were divided into 4 groups: saline-IgG, saline-nAb, DOX-IgG, and DOX-nAb ( N = 10 ). Cardiac injury, cardiomyocyte apoptosis, inflammatory factors, and the biomarkers of M1 and M2 macrophages in each group were analyzed. Result. DOX administration increased the expression of resistin. DOX treatment exacerbated the loss of body and heart weight and cardiac vacuolation in mice. The antiresistin nAb reversed these conditions, downregulated the expression of myocardial injury markers, and decreased apoptosis. In addition, the antiresistin nAb decreased p65 pathway activation, decreased M1 macrophage differentiation and the expression of related inflammatory factors, and increased M2 macrophage differentiation and the expression of related inflammatory factors. Conclusion. The antiresistin nAb protected against DOX-induced cardiac injury by reducing cardiac inflammation and may be a promising target to relieve DOX-related cardiac injury.

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Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance

Gawałko

Saljic

et al. 2022

Cardiovascular Research

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Obesity is an important contributing factor to the pathophysiology of atrial fibrillation (AF) and its complications by causing systemic changes, such as altered haemodynamic, increased sympathetic tone, and low-grade chronic inflammatory state. In addition, adipose tissue is a metabolically active organ that comprises various types of fat deposits with discrete composition and localization that show distinct functions. Fatty tissue differentially affects the evolution of AF, with highly secretory active visceral fat surrounding the heart generally having a more potent influence than the rather inert subcutaneous fat. A variety of proinflammatory, profibrotic, and vasoconstrictive mediators are secreted by adipose tissue, particularly originating from cardiac fat, that promote atrial remodelling and increase the susceptibility to AF. In this review, we address the role of obesity-related factors and in particular specific adipose tissue depots in driving AF risk. We discuss the distinct effects of key secreted adipokines from different adipose tissue depots and their participation in cardiac remodelling. The possible mechanistic basis and molecular determinants of adiposity-related AF are discussed, and finally, we highlight important gaps in current knowledge, areas requiring future investigation, and implications for clinical management.

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Inotropic and lusitropic, but not arrhythmogenic, effects of adipocytokine resistin on human atrial myocardium

Cited by 4 publications

References 38 publications

Evidence that resistin acts on the mechanical responses of the mouse gastric fundus

Evidence that resistin acts on the mechanical responses of the mouse gastric fundus

Antiresistin Neutralizing Antibody Alleviates Doxorubicin-Induced Cardiac Injury in Mice

Adiposity-associated atrial fibrillation: molecular determinants, mechanisms, and clinical significance

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