Reactive Oxygen Species (ROS) Signaling in Cardiac Remodeling and Failure

Harvey, Adam; Grieve, David

doi:10.1007/978-3-642-30018-9_50

Cited by 5 publications

(4 citation statements)

References 312 publications

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“…Moreover, PDGF-BB, IL-12, IL-1β, and MIP-1β (macrophage inflammatory protein-1 beta) from immune cells promote the glycolytic process in fibroblasts which provide more ATP and biosynthetic intermediates for excessive production of the ECM, while inhibition of glycolysis attenuates fibroblast activation and cardiac fibrosis ( Chen et al, 2021a ; Feng et al, 2023 ) . Furthermore, enhanced glycolysis in immune cells can lead to increased production of ROS, contributing to oxidative stress and tissue injury, both of which are implicated in cardiac fibrosis ( Harvey et al, 2014 ; Dhalla et al, 2022 ) . Hence, increased glycolysis is considered a hallmark of metabolic reprogramming in most immune cells undergoing rapid activation in response to stimulation of pattern recognition receptors, cytokine receptors, or antigen receptors which amplify the production of inflammatory cytokines ( Figure 3 ).…”

Section: Metabolic Regulation Of Cardiac Homeostasismentioning

confidence: 99%

Cardiac fibrogenesis: an immuno-metabolic perspective

Hoque,

Gbadegoye,

Hassan

et al. 2024

Front. Physiol.

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Cardiac fibrosis is a major and complex pathophysiological process that ultimately culminates in cardiac dysfunction and heart failure. This phenomenon includes not only the replacement of the damaged tissue by a fibrotic scar produced by activated fibroblasts/myofibroblasts but also a spatiotemporal alteration of the structural, biochemical, and biomechanical parameters in the ventricular wall, eliciting a reactive remodeling process. Though mechanical stress, post-infarct homeostatic imbalances, and neurohormonal activation are classically attributed to cardiac fibrosis, emerging evidence that supports the roles of immune system modulation, inflammation, and metabolic dysregulation in the initiation and progression of cardiac fibrogenesis has been reported. Adaptive changes, immune cell phenoconversions, and metabolic shifts in the cardiac nonmyocyte population provide initial protection, but persistent altered metabolic demand eventually contributes to adverse remodeling of the heart. Altered energy metabolism, mitochondrial dysfunction, various immune cells, immune mediators, and cross-talks between the immune cells and cardiomyocytes play crucial roles in orchestrating the transdifferentiation of fibroblasts and ensuing fibrotic remodeling of the heart. Manipulation of the metabolic plasticity, fibroblast–myofibroblast transition, and modulation of the immune response may hold promise for favorably modulating the fibrotic response following different cardiovascular pathological processes. Although the immunologic and metabolic perspectives of fibrosis in the heart are being reported in the literature, they lack a comprehensive sketch bridging these two arenas and illustrating the synchrony between them. This review aims to provide a comprehensive overview of the intricate relationship between different cardiac immune cells and metabolic pathways as well as summarizes the current understanding of the involvement of immune–metabolic pathways in cardiac fibrosis and attempts to identify some of the previously unaddressed questions that require further investigation. Moreover, the potential therapeutic strategies and emerging pharmacological interventions, including immune and metabolic modulators, that show promise in preventing or attenuating cardiac fibrosis and restoring cardiac function will be discussed.

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Section: Metabolic Regulation Of Cardiac Homeostasismentioning

confidence: 99%

Cardiac fibrogenesis: an immuno-metabolic perspective

Hoque,

Gbadegoye,

Hassan

et al. 2024

Front. Physiol.

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“…39 It is well established that ROS negatively affects collagen synthesis, fibroblast proliferation and matrix metalloproteinase (MMP) activity, leading to myocardial hypertrophy, fibrosis, necrosis and endothelial dysfunction. 36,40,41 Overproduction of ROS also leads to increased generation of O For instance, upregulation of XO could lead to energetic disturbances in myocardial cells, and NOX induces changes in cardiac pathophysiology through stimulation of redox-sensitive kinases. 36,42,43 Studies have proposed that the generation of mitochondrial ROS may be linked to cardiac dysfunction due to the high concentrations of mitochondria in heart tissue.…”

Section: The Role Of Os In Cvdsmentioning

confidence: 99%

“…In cardiomyocytes, ROS directly interferes with the electrophysiology and contraction machinery by altering proteins related to excitation–contraction coupling, including Na + channels, K + channels, Ca 2+ channels and Na + /Ca 2+ exchangers 39 . It is well established that ROS negatively affects collagen synthesis, fibroblast proliferation and matrix metalloproteinase (MMP) activity, leading to myocardial hypertrophy, fibrosis, necrosis and endothelial dysfunction 36,40,41 . Overproduction of ROS also leads to increased generation of O 2 •‐ and H 2 O 2 in HF by the enzymatic sources, for example, lipooxygenase, xanthine oxidase (XO), cyclooxygenase, uncoupled nitric oxide synthases (NOS), and NADPH oxidase (NOX).…”

Section: Cardiovascular Diseasesmentioning

confidence: 99%

Cardioprotective potential of vanillic acid

Yalameha

Nejabati

Nouri

2022

Clin Exp Pharma Physio

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Nowadays, cardiovascular diseases (CVDs) are a global threat to public health, accounting for almost one‐third of all deaths worldwide. One of the key mechanistic pathways contributing to the development of CVDs, including cardiotoxicity (CTX) and myocardial ischaemia–reperfusion injury (MIRI) is oxidative stress (OS). Increased generation of reactive oxygen species (ROS) is closely associated with decreased antioxidant capacity and mitochondrial dysfunction. Currently, despite the availability of modern pharmaceuticals, dietary‐derived antioxidants are becoming more popular in developed societies to delay the progression of CVDs. One of the antioxidants derived from herbs, fruits, whole grains, juices, beers, and wines is vanillic acid (VA), which, as a phenolic compound, possesses different therapeutic properties, including cardioprotective. Based on experimental evidence, VA improves mitochondrial function as a result of the reduction in ROS production, aggravates antioxidative status, scavenges free radicals, and reduces levels of lipid peroxidation, thereby decreasing cardiac dysfunction, in particular CTX and MIRI. Considering the role of OS in the pathophysiology of CVDs, the purpose of this study is to comprehensively address recent evidence on the antioxidant importance of VA in the cardiovascular system.

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“…Polymorphonuclear neutrophils, macrophages, and other cells involved in the host-defense produce reactive oxygen species (ROS), , partially reduced metabolites of oxygen that possess strong oxidizing capabilities that play an important role as complex signaling functions − in the progress of inflammatory disorders. However, enhanced ROS generation at the site of inflammation causes oxidative stress, an imbalance between ROS production and the ability to detoxify the reactive oxygen intermediates. − Chronic or prolonged ROS production is interrelated with the progress of inflammatory diseases, and in such cases the wound can become chronic or progressively fibrotic; both outcomes impair tissue function …”

Section: Introductionmentioning

confidence: 99%

Electrospun Fibers of Polyester, with Both Nano- and Micron Diameters, Loaded with Antioxidant for Application as Wound Dressing or Tissue Engineered Scaffolds

Fernández¹,

Ruiz-Ruiz²,

Sarasua

2019

ACS Appl. Polym. Mater.

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Antioxidant loaded poly(ε-caprolactone) (PCL) scaffolds were fabricated by electrospinning and then tested – mechanically and characterized via microscopy imaging. These mats are intended to be used in tissue repair or for wound healing, and their aim is to enhance the biocompatibility by reducing the inflammatory response related to biomaterials via the release of reactive oxygen species, (ROS)-responsive molecules, with antifibrotic properties over a certain length of time. Of the antioxidants studied, only allicin, curcumin, piperine, polydatin, and quercetin were found to be miscible with the polyester and gave rise to better processing by electrospinning and a greater homogeneity of the mats. The scaffolds of different fiber morphologies (micro-, nano-, or micronanostructured, the latter more closely mimicking the structure of the extracellular matrix of soft tissue) filled with 5% of antioxidant, showed a Young’s modulus and tensile strengths lower than those of pure PCL (i.e., elastic modulus of 5–9 MPa vs 12–27 MPa for PCL) but exhibited very interesting mechanical behavior for soft tissue engineered applications with elongation at breaks higher than 25% at room temperature. In a preliminary study, human adipose-derived mesenchymal stem cells were also seeded in several scaffolds and analyzed by fluorescence microscopy and showed that the cells were able to attach, survive, and grow in these 3D culture systems.

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Reactive Oxygen Species (ROS) Signaling in Cardiac Remodeling and Failure

Cited by 5 publications

References 312 publications

Cardiac fibrogenesis: an immuno-metabolic perspective

Cardiac fibrogenesis: an immuno-metabolic perspective

Cardioprotective potential of vanillic acid

Electrospun Fibers of Polyester, with Both Nano- and Micron Diameters, Loaded with Antioxidant for Application as Wound Dressing or Tissue Engineered Scaffolds

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