NETosis Is Required for S100A8/A9-Induced Granulopoiesis After Myocardial Infarction

Nagareddy, Prabhakara R; Sreejit, Gopalkrishna; Abo-Aly, Mohamed; Jaggers, Robert M; Chelvarajan, Lakshman; Johnson, Jillian; Pernes, Gerard; Athmanathan, Baskaran; Abdel‐Latif, Ahmed; Murphy, Andrew

doi:10.1161/atvbaha.120.314807

Cited by 36 publications

(36 citation statements)

References 5 publications

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“…It is now understood that the induction of myocardial infarction leads to the rapid recruitment of neutrophils to the infarct, where they release the alarm protein S100A8/A9 and bind to TLR-4 to activate the naive neutrophil NLR family pyrin domain containing 3 inflammasome and promote IL-1 β secretion. The released IL-1 β stimulates the autonomous granulocyte production of hematopoietic stem cells in the bone marrow, which requires NETosis [ 136 , 137 ].…”

Section: Damage-associated Molecular Patterns and Cytokines Linkinmentioning

confidence: 99%

NETosis as a Pathogenic Factor for Heart Failure

Ling

2021

Oxidative Medicine and Cellular Longevity

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Heart failure threatens the lives of patients and reduces their quality of life. Heart failure, especially heart failure with preserved ejection fraction, is closely related to systemic and local cardiac persistent chronic low-grade aseptic inflammation, microvascular damage characterized by endothelial dysfunction, oxidative stress, myocardial remodeling, and fibrosis. However, the initiation and development of persistent chronic low-grade aseptic inflammation is unexplored. Oxidative stress-mediated neutrophil extracellular traps (NETs) are the main immune defense mechanism against external bacterial infections. Furthermore, NETs play important roles in noninfectious diseases. After the onset of myocardial infarction, atrial fibrillation, or myocarditis, neutrophils infiltrate the damaged tissue and aggravate inflammation. In tissue injury, damage-related molecular patterns (DAMPs) may induce pattern recognition receptors (PRRs) to cause NETs, but whether NETs are directly involved in the pathogenesis and development of heart failure and the mechanism is still unclear. In this review, we analyzed the markers of heart failure and heart failure-related diseases and comorbidities, such as mitochondrial DNA, high mobility box group box 1, fibronectin extra domain A, and galectin-3, to explore their role in inducing NETs and to investigate the mechanism of PRRs, such as Toll-like receptors, receptor for advanced glycation end products, cGAS-STING, and C-X-C motif chemokine receptor 2, in activating NETosis. Furthermore, we discussed oxidative stress, especially the possibility that imbalance of thiol redox and MPO-derived HOCl promotes the production of 2-chlorofatty acid and induces NETosis, and analyzed the possibility of NETs triggering coronary microvascular thrombosis. In some heart diseases, the deletion or blocking of neutrophil-specific myeloperoxidase and peptidylarginine deiminase 4 has shown effectiveness. According to the results of current pharmacological studies, MPO and PAD4 inhibitors are effective at least for myocardial infarction, atherosclerosis, and certain autoimmune diseases, whose deterioration can lead to heart failure. This is essential for understanding NETosis as a therapeutic factor of heart failure and the related new pathophysiology and therapeutics of heart failure.

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Section: Damage-associated Molecular Patterns and Cytokines Linkinmentioning

confidence: 99%

NETosis as a Pathogenic Factor for Heart Failure

Ling

2021

Oxidative Medicine and Cellular Longevity

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“…is conducive for both activation of neutrophils and cell death by NETosis. It is likely that NETosis is essential for S100A8/A9 release in the heart post-MI (61).…”

Section: Granulopoiesis During Myocardial Infarction: Role Of Dampsmentioning

confidence: 99%

Emerging roles of neutrophil-borne S100A8/A9 in cardiovascular inflammation

Sreejit

Latif

Murphy

et al. 2020

Pharmacological Research

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“…Intriguingly, the effects of diabetes on myelopoiesis are prevented by elevating HDL levels, suggesting that the mechanism whereby diabetes increases myelopoiesis can be blunted by cholesterol efflux (Barrett et al, 2019) and therefore is dependent on lipid alterations. Other studies have placed NETosis upstream of release of S100A9 from neutrophils and subsequent granulopoiesis (Nagareddy et al, 2020) (Figure 2). NETosis is a form of neutrophil death characterized by release of decondensed chromatin and granular materials to aid in the trapping and killing of pathogens.…”

Section: Suppression Of Inflammatory Processes Is Beneficial In Animal Models Of Diabetes-exacerbated Atherosclerosismentioning

confidence: 99%