Heart Inflammation

Carrillo‐Salinas, Francisco; Ngwenyama, Njabulo; Anastasiou, Marina; Kaur, Kuljeet; Alcaide, Pilar

doi:10.1016/j.ajpath.2019.04.009

Cited by 87 publications

(31 citation statements)

References 100 publications

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“…When the aorta was constricted, fluctuation and overload of blood pressure activated the renin-angiotensin-aldosterone system (RAAS), which initiates a cascade reaction of neurohormone regulation [ 22 ]; in this condition, cardiomyocytes and cardiac fibroblasts would release TNF- α and IL-6 [ 22 , 30 ]. The proinflammatory cytokines would orchestrate the expression of cytokines and chemokines and thus promotes the injury of resident interstitial cells and the recruitment of immune cells [ 22 , 31 , 32 ]. The accumulation of abundant inflammatory factors and inflammatory cells provides an inflammatory microenvironment for cardiac remodeling and heart failure.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] Alleviation of Inflammation and Oxidative Stress in Pressure Overload‐Induced Cardiac Remodeling and Heart Failure via IL‐6/STAT3 Inhibition by Raloxifene

Huo

Shi

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. Inflammation and oxidative stress are involved in the initiation and progress of heart failure (HF). However, the role of the IL6/STAT3 pathway in the pressure overload-induced HF remains controversial. Methods and Results. Transverse aortic constriction (TAC) was used to induce pressure overload-HF in C57BL/6J mice. 18 mice were randomized into three groups (Sham, TAC, and TAC+raloxifene, n = 6 , respectively). Echocardiographic and histological results showed that cardiac hypertrophy, fibrosis, and left ventricular dysfunction were manifested in mice after TAC treatment of eight weeks, with aggravation of macrophage infiltration and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression in the myocardium. TAC (four and eight weeks) elevated the phosphorylation of signal transducer and activator of transcription 3 (p-STAT3) and prohibitin2 (PHB2) protein expression. Importantly, IL-6/gp130/STAT3 inhibition by raloxifene alleviated TAC-induced myocardial inflammation, cardiac remodeling, and dysfunction. In vitro, we demonstrated cellular hypertrophy with STAT3 activation and oxidative stress exacerbation could be elicited by IL-6 (25 ng/mL, 48 h) in H9c2 myoblasts. Sustained IL-6 stimulation increased intracellular reactive oxygen species, repressed mitochondrial membrane potential (MMP), decreased intracellular content of ATP, and led to decreased SOD activity, an increase in iNOS protein expression, and increased protein expression of Pink1, Parkin, and Bnip3 involving in mitophagy, all of which were reversed by raloxifene. Conclusion. Inflammation and IL-6/STAT3 signaling were activated in TAC-induced HF in mice, while sustained IL-6 incubation elicited oxidative stress and mitophagy-related protein increase in H9c2 myoblasts, all of which were inhibited by raloxifene. These indicated IL-6/STAT3 signaling might be involved in the pathogenesis of myocardial hypertrophy and HF.

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Section: Discussionmentioning

confidence: 99%

[Retracted] Alleviation of Inflammation and Oxidative Stress in Pressure Overload‐Induced Cardiac Remodeling and Heart Failure via IL‐6/STAT3 Inhibition by Raloxifene

Huo

Shi

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…This conclusion is further supported by the expression of genes encoding the pro-inflammatory cytokines Il1b, Il6, Tnfa and the chemokine Ccl2. This initial pro-inflammatory period resolves within a few days and is followed by a reparative phase dominated by macrophages, lymphocytes, and proliferating scar-forming myofibroblasts 13,14,[20][21][22]30 . The absence of B and T lymphocytes at 2 d after reperfusion further supports the conclusion that CMC injection occurred during the initial pro-inflammatory phase.…”

Section: Discussionmentioning

confidence: 99%

Administration of cardiac mesenchymal cells modulates innate immunity in the acute phase of myocardial infarction in mice

Kang

Nasr

Guo

et al. 2020

Sci Rep

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Although cardiac mesenchymal cell (CMC) therapy mitigates post-infarct cardiac dysfunction, the underlying mechanisms remain unidentified. It is acknowledged that donor cells are neither appreciably retained nor meaningfully contribute to tissue regeneration—suggesting a paracrine-mediated mechanism of action. As the immune system is inextricably linked to wound healing/remodeling in the ischemically injured heart, the reparative actions of CMCs may be attributed to their immunoregulatory properties. The current study evaluated the consequences of CMC administration on post myocardial infarction (MI) immune responses in vivo and paracrine-mediated immune cell function in vitro. CMC administration preferentially elicited the recruitment of cell types associated with innate immunity (e.g., monocytes/macrophages and neutrophils). CMC paracrine signaling assays revealed enhancement in innate immune cell chemoattraction, survival, and phagocytosis, and diminished pro-inflammatory immune cell activation; data that identifies and catalogues fundamental immunomodulatory properties of CMCs, which have broad implications regarding the mechanism of action of CMCs in cardiac repair.

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“…Recent studies indicate that at later stages T regs become dysfunctional, taking on proinflammatory and antiangiogenic properties (9). Another subset of T cells, termed T-helper (Th) cells, also expand in the spleen and migrate to the heart during development of ischemic heart failure, with Th17 and Th2 subsets contributing to the progression to heart failure (12).…”

Section: Monocyte/macrophage and T-cell Recruitmentmentioning

confidence: 99%

“…The site of immune T-cell activation also differs, occurring in the mediastinal lymph node following TAC versus the spleen in response to MI. Growing evidence supports a role for T cells in later stages of heart failure as strategies for blocking their activation and recruitment have salutary effects on TAC-induced adverse remodeling (12,48).…”

Section: Monocyte/macrophage Accumulationmentioning

confidence: 99%

Inflammation in nonischemic heart disease: initiation by cardiomyocyte CaMKII and NLRP3 inflammasome signaling

Suetomi

Miyamoto

Brown

2019

American Journal of Physiology-Heart and Circulatory Physiology

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There is substantial evidence that chronic heart failure in humans and in animal models is associated with inflammation. Ischemic interventions such as myocardial infarction lead to necrotic cell death and release of damage associated molecular patterns, factors that signal cell damage and induce expression of proinflammatory chemokines and cytokines. It has recently become evident that nonischemic interventions are also associated with increases in inflammatory genes and immune cell accumulation in the heart and that these contribute to fibrosis and ventricular dysfunction. How proinflammatory responses are elicited in nonischemic heart disease which is not, at least initially, associated with cell death is a critical unanswered question. In this review we provide evidence supporting the hypothesis that cardiomyocytes are an initiating site of inflammatory gene expression in response to nonischemic stress. Furthermore we discuss the role of the multifunctional Ca2+/calmodulin-regulated kinase, CaMKIIδ, as a transducer of stress signals to nuclear factor-κB activation, expression of proinflammatory cytokines and chemokines, and priming and activation of the NOD-like pyrin domain-containing protein 3 (NLRP3) inflammasome in cardiomyocytes. We summarize recent evidence that subsequent macrophage recruitment, fibrosis and contractile dysfunction induced by angiotensin II infusion or transverse aortic constriction are ameliorated by blockade of CaMKII, of monocyte chemoattractant protein-1/C-C chemokine receptor type 2 signaling, or of NLRP3 inflammasome activation.

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Heart Inflammation

Abstract: recognizes early career investigators with demonstrated excellence as an investigator with recently established or emerging independence and with a research focus leading to an improved understanding of the conceptual basis of disease.

Cited by 87 publications

References 100 publications

[Retracted] Alleviation of Inflammation and Oxidative Stress in Pressure Overload‐Induced Cardiac Remodeling and Heart Failure via IL‐6/STAT3 Inhibition by Raloxifene

[Retracted] Alleviation of Inflammation and Oxidative Stress in Pressure Overload‐Induced Cardiac Remodeling and Heart Failure via IL‐6/STAT3 Inhibition by Raloxifene

Administration of cardiac mesenchymal cells modulates innate immunity in the acute phase of myocardial infarction in mice

Inflammation in nonischemic heart disease: initiation by cardiomyocyte CaMKII and NLRP3 inflammasome signaling

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