Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection

Heusch, Gerd; Andreadou, Ioanna; Bell, Robert; Bertero, Edoardo; Botker, Hans-Erik; Davidson, Sean M.; Downey, James; Eaton, Philip; Ferdinandy, Peter; Gersh, Bernard J.; Giacca, Mauro; Hausenloy, Derek J.; Ibanez, Borja; Krieg, Thomas; Maack, Christoph; Schulz, Rainer; Sellke, Frank; Shah, Ajay M.; Thiele, Holger; Yellon, Derek M.; Di Lisa, Fabio

doi:10.1016/j.redox.2023.102894

Cited by 30 publications

(10 citation statements)

References 600 publications

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“…Clinical and epidemiological data also show an association between typical oxidative stress markers, such as lipid peroxidation products, 3-nitrotyrosine or oxidized DNA/RNA bases, with all significant non-communicable diseases of cardiovascular [ [343] , [344] , [345] ], metabolic [ 39 , 40 ] or neurodegenerative origin [ 42 , 346 ] as well as with different forms of cancer [ 41 , 347 ]. Especially ischemic heart disease is tightly linked to mitochondrial H 2 O 2 /O 2 •− formation and oxidative tissue damage [ 348 ]. Since oxidative stress is a hallmark of most non-communicable diseases, it is important to know more about the sources of H 2 O 2 /O 2 •− , and to gain insight into the mechanisms of oxidative damage, thereby providing better understanding of noise-induced diseases described in the first part of this position paper.…”

Section: Pathophysiological Mechanisms Of Noise Exposurementioning

confidence: 99%

Health position paper and redox perspectives - Disease burden by transportation noise

Sørensen,

Pershagen,

Thacher

et al. 2024

Redox Biology

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Section: Pathophysiological Mechanisms Of Noise Exposurementioning

confidence: 99%

Health position paper and redox perspectives - Disease burden by transportation noise

Sørensen,

Pershagen,

Thacher

et al. 2024

Redox Biology

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“…Cardiac I/R injury is a complex process wherein neutrophils recruit more in ammatory cells and release pathogenic proteases, including matrix metalloproteinases, chemotactic factors, and myeloperoxidase (MPO), which exacerbate cardiac injury in the infarcted myocardium [6,7]. Furthermore, it has been demonstrated that NETs formation, characterized by the release of web-like structures during neutrophil cell death, also contributes to the in ammatory damage process in myocardial infarction [8,9].…”

Section: Introductionmentioning

confidence: 99%

Blocking the TRAIL-DR5 pathway reduces cardiac ischemia-reperfusion injury by decreasing neutrophil infiltration and neutrophil extracellular traps formation

Wang,

Xie,

Zhao

et al. 2024

Preprint

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Purpose Acute myocardial infarction (AMI) is a leading cause of mortality. Neutrophils penetrate injured heart tissue during AMI or ischemia-reperfusion (I/R) injury and produce inflammatory factors, chemokines, and extracellular traps that exacerbate heart injury. Inhibition of the TRAIL-DR5 pathway has been demonstrated to alleviate cardiac ischemia-reperfusion injury in a leukocyte-dependent manner. However, it remains unknown whether TRAIL-DR5 signaling is involved in regulating neutrophil extracellular traps (NETs) release. Methods This study used various models to examine the effects of activating the TRAIL-DR5 pathway with soluble mouse TRAIL protein and inhibiting the TRAIL-DR5 signaling pathway using DR5 knockout mice or mDR5-Fc fusion protein on NETs formation and cardiac injury. The models used included a co-culture model involving bone marrow-derived neutrophils and primary cardiomyocytes and a model of myocardial I/R in mice. Results NETs formation is suppressed by TRAIL-DR5 signaling pathway inhibition, which can lessen cardiac ischemia-reperfusion injury. This intervention reduces adhesion molecules and chemokines releasing, resulting in decreased neutrophil infiltration and inhibiting NETs production by downregulating PAD4 in neutrophils. Conclusion This work clarifies how the TRAIL-DR5 signaling pathway regulates the neutrophil response during myocardial I/R damage, thereby providing a scientific basis for therapeutic intervention targeting the TRAIL-DR5 signaling pathway in myocardial infarction.

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“…Moreover, hypertension [18,43] and T2DM [4,46] trigger inflammation, an independent cardiovascular risk factor [22,45]. Inflammation and oxidative stress are known to enhance each other in a cross-talk fashion [11,44] and prevention of excessive reactive oxygen species is a hallmark of most cardioprotective therapies [21].…”

Section: Introductionmentioning

confidence: 99%

Role of inflammatory signaling pathways involving the CD40–CD40L–TRAF cascade in diabetes and hypertension—insights from animal and human studies

Strohm,

Daiber,

Ubbens

et al. 2024

Basic Res Cardiol

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CD40L–CD40–TRAF signaling plays a role in atherosclerosis progression and affects the pathogenesis of coronary heart disease (CHD). We tested the hypothesis that CD40L–CD40–TRAF signaling is a potential therapeutic target in hyperlipidemia, diabetes, and hypertension. In mouse models of hyperlipidemia plus diabetes (db/db mice) or hypertension (1 mg/kg/d angiotensin-II for 7 days), TRAF6 inhibitor treatment (2.5 mg/kg/d for 7 or 14 days) normalized markers of oxidative stress and inflammation. As diabetes and hypertension are important comorbidities aggravating CHD, we explored whether the CD40L–CD40–TRAF signaling cascade and their associated inflammatory pathways are expressed in CHD patients suffering from comorbidities. Therefore, we analyzed vascular bypass material (aorta or internal mammary artery) and plasma from patients with CHD with diabetes and/or hypertension. Our Olink targeted plasma proteomic analysis using the IMMUNO-ONCOLOGY panel revealed a pattern of step-wise increase for 13/92 markers of low-grade inflammation with significant changes. CD40L or CD40 significantly correlated with 38 or 56 other inflammatory targets. In addition, specific gene clusters that correlate with the comorbidities were identified in isolated aortic mRNA of CHD patients through RNA-sequencing. These signaling clusters comprised CD40L–CD40–TRAF, immune system, hemostasis, muscle contraction, metabolism of lipids, developmental biology, and apoptosis. Finally, immunological analysis revealed key markers correlated with comorbidities in CHD patients, such as CD40L, NOX2, CD68, and 3-nitrotyrosine. These data indicate that comorbidities increase inflammatory pathways in CHD, and targeting these pathways will be beneficial in reducing cardiovascular events in CHD patients with comorbidities.

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Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection

Cited by 30 publications

References 600 publications

Health position paper and redox perspectives - Disease burden by transportation noise

Health position paper and redox perspectives - Disease burden by transportation noise

Blocking the TRAIL-DR5 pathway reduces cardiac ischemia-reperfusion injury by decreasing neutrophil infiltration and neutrophil extracellular traps formation

Role of inflammatory signaling pathways involving the CD40–CD40L–TRAF cascade in diabetes and hypertension—insights from animal and human studies

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