Nifedipine inhibits the activation of inflammatory and immune reactions in viral myocarditis

Liu, Wenjun; Shimada, Miho; Xiao, Jie; Hu, Dayi; Matsumori, Akira

doi:10.1016/j.lfs.2009.05.018

Cited by 13 publications

(3 citation statements)

References 40 publications

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“…It can thus be hypothesized that elevation of calcium concentration in steroidogenic CACNA1D-mutated cells might upregulate expression of SCF reinforcing mast cell chemoattraction in adrenal lesions. In support of this assumption, it has been reported that the L-type calcium channel blocker nifedipine reduces expression of SCF and lowers cardiac mast cell density in a mouse model of viral myocarditis [85]. It is also conceivable that aldosterone overproduction may activate adrenal mast cells, since this cell type is known to express the mineralocorticoid receptor [86,87].…”

Section: Mast Cells In Pathophysiology Of Hyperaldosteronismmentioning

confidence: 94%

Role of Mast Cells in the Control of Aldosterone Secretion

et al. 2020

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Mast cells are immune cells present in adrenals from various species. Proliferation and activation of adrenal mast cells seem to be influenced by environment, since they increase during summer and in response to sodium restriction in frogs and mouse, respectively. Although the physiological factors regulating adrenal mast cell activity have not been identified, they might involve neurotransmitters and the renin-angiotensin system. Some data indicate that adrenal mast cells stimulate proliferation of steroidogenic cells in the zona glomerulosa and activate the mineralocorticoid production. In human, mast cell degranulation stimulates aldosterone synthesis through the release of serotonin (5-HT) and activation of 5-HT4 receptors. Increase in mast cell population and upregulation of the 5-HT signaling pathway occur in aldosterone-producing adenomas. In particular, aldosterone-producing adenoma cells overexpress 5-HT4 receptors and are hyper-responsive to 5-HT4 receptor agonists. These data suggest that the intra-adrenal serotonergic regulatory system represents a potential target for development of both adrenal imaging methods to evaluate the lateralization of aldosterone production, and pharmacological treatments of primary aldosteronism.

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Section: Mast Cells In Pathophysiology Of Hyperaldosteronismmentioning

confidence: 94%

Role of Mast Cells in the Control of Aldosterone Secretion

et al. 2020

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“…Digoxin should be used with caution and only in low doses in patients with viral myocarditis because administration of digoxin in high doses to mice with viral-induced myocarditis increased mortality. 144 Amlodipine improved survival, ratio of heart weight to body weight, and the histopathologic grades of myocardial lesions in one study in a murine model of viral myocarditis, 145 whereas nifedipine decreased the activation of proinflammatory cytokines in another study in mice with viral myocarditis 146 ; however, no data on use of calcium channel blockers in humans with viral myocarditis has been published. Patients with high filling pressures may require support with intravenous vasodilators, whereas patients who present with severe symptoms may require intravenous inotropic medications.…”

Section: Treatmentmentioning

confidence: 99%

Myocarditis

Blauwet

Cooper

2010

Progress in Cardiovascular Diseases

358

316

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Myocarditis is an uncommon, potentially life-threatening disease that presents with a wide range of symptoms in children and adults. Viral infection is the most common cause of myocarditis in developed countries, but other etiologies include bacterial and protozoal infections, toxins, drug reactions, autoimmune diseases, giant cell myocarditis, and sarcoidosis. Acute injury leads to myocyte damage, which in turn activates the innate and humeral immune system, leading to severe inflammation. In most patients, the immune reaction is eventually down-regulated and the myocardium recovers. In select cases, however, persistent myocardial inflammation leads to ongoing myocyte damage and relentless symptomatic heart failure or even death. The diagnosis is usually made based on clinical presentation and noninvasive imaging findings. Most patients respond well to standard heart failure therapy, although in severe cases, mechanical circulatory support or heart transplantation is indicated. Prognosis in acute myocarditis is generally good except in patients with giant cell myocarditis. Persistent, chronic myocarditis usually has a progressive course but may respond to immunosuppression.

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“…The main characteristics of included studies, and their references, are given in Supplementary material. All studies used hematoxylin and eosin (HE) staining for inflammation, calcification and necrosis, except for the study by Liu et al that used Masson’s trichrome to measure necrosis [43]. Studies used one of three stains for fibrosis: Masson’s trichrome, Azan-Mallory or HE.…”

Section: Resultsmentioning

confidence: 99%

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

et al. 2019

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Current myocarditis guidelines do not advocate treatment to prevent myocardial injury and scar deposition in patients with myocarditis and normal left ventricular ejection fraction. We aimed to ascertain the utility of beta blockers, calcium channel blockers and antagonists of the renin–angiotensin system in ameliorating myocardial injury, scar formation and calcification in animal in vivo models of myocarditis. The project was prospectively registered with the PROSPERO database of systematic reviews (CRD42018089336). Primary outcomes (necrosis, fibrosis and calcification) were meta-analysed with random-effects modelling. 52 studies were systematically reviewed. Meta-analysis was performed compared with untreated controls. In each study, we identified all independent comparisons of treatment versus control groups. The pooled weighted mean difference (WMD) indicated treatment reduced necrosis by 16.9% (71 controlled analyses, 95% CI 13.2–20.7%; P < 0.001), however there was less evidence of an effect after accounting for publication bias. Treatment led to a 12.8% reduction in fibrosis (73 controlled analyses, 95% CI 7.6–18.0%; P < 0.001). After accounting for publication bias this was attenuated to 7.8% but remained significant. Treatment reduced calcification by 4.1% (28 controlled analyses, 95% CI 0.2–8.0%; P < 0.0395). We observed significant heterogeneity in effect size in all primary endpoints, which was predominantly driven by differences between drug categories. Beta blockers and angiotensin-converting enzyme (ACE) inhibitors were the only agents that were effective for both necrosis and fibrosis, while only ACE inhibitors had a significant effect on calcification. This study provides evidence for a role for ACE inhibitors and beta blockers to prevent myocardial injury and scar deposition in in vivo models of myocarditis. There is a need for further well-designed studies to assess the translational application of these treatments.Electronic supplementary materialThe online version of this article (10.1007/s00395-019-0754-x) contains supplementary material, which is available to authorized users.

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Nifedipine inhibits the activation of inflammatory and immune reactions in viral myocarditis

Cited by 13 publications

References 40 publications

Role of Mast Cells in the Control of Aldosterone Secretion

Role of Mast Cells in the Control of Aldosterone Secretion

Myocarditis

Therapies to limit myocardial injury in animal models of myocarditis: a systematic review and meta-analysis

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