The Role of Redox Signalling in Cardiovascular Regeneration

2019 ◽  
pp. 19-37
Author(s):  
Thomas Hansen ◽  
Soloman Saleh ◽  
Gemma A. Figtree ◽  
Carmine Gentile
Keyword(s):  
Redox Signalling ◽  
Cardiovascular Regeneration

scholarly journals Roles of Autophagy in Oxidative Stress

2020 ◽  
Vol 21 (9) ◽  
pp. 3289 ◽  
Author(s):  
Hyeong Rok Yun ◽  
Yong Hwa Jo ◽  
Jieun Kim ◽  
Yoonhwa Shin ◽  
Sung Soo Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Stress Responses ◽  
Basic Mechanism ◽  
Redox Signalling ◽  
Mitochondrial Ros ◽  
Related Stress ◽  
And Function ◽  
Catabolic Process

Autophagy is a catabolic process for unnecessary or dysfunctional cytoplasmic contents by lysosomal degradation pathways. Autophagy is implicated in various biological processes such as programmed cell death, stress responses, elimination of damaged organelles and development. The role of autophagy as a crucial mediator has been clarified and expanded in the pathological response to redox signalling. Autophagy is a major sensor of the redox signalling. Reactive oxygen species (ROS) are highly reactive molecules that are generated as by-products of cellular metabolism, principally by mitochondria. Mitochondrial ROS (mROS) are beneficial or detrimental to cells depending on their concentration and location. mROS function as redox messengers in intracellular signalling at physiologically low level, whereas excessive production of mROS causes oxidative damage to cellular constituents and thus incurs cell death. Hence, the balance of autophagy-related stress adaptation and cell death is important to comprehend redox signalling-related pathogenesis. In this review, we attempt to provide an overview the basic mechanism and function of autophagy in the context of response to oxidative stress and redox signalling in pathology.

scholarly journals The Role of Free Radicals in Autophagy Regulation: Implications for Ageing

2018 ◽  
Vol 2018 ◽  
pp. 1-19 ◽  
Author(s):  
M. Pajares ◽  
A. Cuadrado ◽  
N. Engedal ◽  
Z. Jirsova ◽  
M. Cahova
Keyword(s):  
Control Systems ◽  
Redox Homeostasis ◽  
Biological Macromolecules ◽  
Complex Relationship ◽  
Cellular Functions ◽  
Related Disorder ◽  
Redox Signalling ◽  
Age Related ◽  
Integral Role

Reactive oxygen and nitrogen species (ROS and RNS, resp.) have been traditionally perceived solely as detrimental, leading to oxidative damage of biological macromolecules and organelles, cellular demise, and ageing. However, recent data suggest that ROS/RNS also plays an integral role in intracellular signalling and redox homeostasis (redoxtasis), which are necessary for the maintenance of cellular functions. There is a complex relationship between cellular ROS/RNS content and autophagy, which represents one of the major quality control systems in the cell. In this review, we focus on redox signalling and autophagy regulation with a special interest on ageing-associated changes. In the last section, we describe the role of autophagy and redox signalling in the context of Alzheimer’s disease as an example of a prevalent age-related disorder.

scholarly journals The Redox System inC. elegans, a Phylogenetic Approach

2012 ◽  
Vol 2012 ◽  
pp. 1-20 ◽  
Author(s):  
Andrew D. Johnston ◽  
Paul R. Ebert
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Cellular Damage ◽  
Future Research ◽  
Homologous Proteins ◽  
Redox Biology ◽  
Redox Signalling ◽  
C Elegans ◽  
Age Related

Oxidative stress is a toxic state caused by an imbalance between the production and elimination of reactive oxygen species (ROS). ROS cause oxidative damage to cellular components such as proteins, lipids, and nucleic acids. While the role of ROS in cellular damage is frequently all that is noted, ROS are also important in redox signalling. The “Redox Hypothesis" has been proposed to emphasize a dual role of ROS. This hypothesis suggests that the primary effect of changes to the redox state is modified cellular signalling rather than simply oxidative damage. In extreme cases, alteration of redox signalling can contribute to the toxicity of ROS, as well as to ageing and age-related diseases. The nematode speciesCaenorhabditis elegansprovides an excellent model for the study of oxidative stress and redox signalling in animals. We use protein sequences from central redox systems inHomo sapiens,Drosophila melanogaster, andSaccharomyces cerevisiaeto query Genbank for homologous proteins inC. elegans. We then use maximum likelihood phylogenetic analysis to compare protein families betweenC. elegansand the other organisms to facilitate future research into the genetics of redox biology.

scholarly journals Human Induced Pluripotent Stem Cell-Derived Vascular Cells: Recent Progress and Future Directions

2021 ◽  
Vol 8 (11) ◽  
pp. 148
Author(s):  
Jee Eun Oh ◽  
Cholomi Jung ◽  
Young-sup Yoon
Keyword(s):  
Animal Models ◽  
Induced Pluripotent Stem Cell ◽  
Great Promise ◽  
Vascular Cells ◽  
Future Directions ◽  
Tissue Repair And Regeneration ◽  
Therapeutic Benefits ◽  
Cardiovascular Regeneration ◽  
Induced Pluripotent

Human induced pluripotent stem cells (hiPSCs) hold great promise for cardiovascular regeneration following ischemic injury. Considerable effort has been made toward the development and optimization of methods to differentiate hiPSCs into vascular cells, such as endothelial and smooth muscle cells (ECs and SMCs). In particular, hiPSC-derived ECs have shown robust potential for promoting neovascularization in animal models of cardiovascular diseases, potentially achieving significant and sustained therapeutic benefits. However, the use of hiPSC-derived SMCs that possess high therapeutic relevance is a relatively new area of investigation, still in the earlier investigational stages. In this review, we first discuss different methodologies to derive vascular cells from hiPSCs with a particular emphasis on the role of key developmental signals. Furthermore, we propose a standardized framework for assessing and defining the EC and SMC identity that might be suitable for inducing tissue repair and regeneration. We then highlight the regenerative effects of hiPSC-derived vascular cells on animal models of myocardial infarction and hindlimb ischemia. Finally, we address several obstacles that need to be overcome to fully implement the use of hiPSC-derived vascular cells for clinical application.

The role of NADPH oxidase in cocaine-induced cardiac oxidative stress and redox signalling

2008 ◽  
Vol 44 (4) ◽  
pp. 713 ◽  
Author(s):  
Lampson Fan ◽  
David Sawbridge ◽  
Alexis Bailey ◽  
Ian Kitchen ◽  
Jian-Mei Li
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Redox Signalling

Hepatocyte growth factor: Molecular biomarker and player in cardioprotection and cardiovascular regeneration

2012 ◽  
Vol 107 (04) ◽  
pp. 656-661 ◽  
Author(s):  
Rosalinda Madonna ◽  
Cihan Cevik ◽  
Maher Nasser ◽  
Raffaele De Caterina
Keyword(s):  
Myocardial Infarction ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Cell Types ◽  
Diagnostic Biomarker ◽  
Scatter Factor ◽  
Molecular Biomarker ◽  
Cardiovascular Regeneration ◽  
Hepatocyte Growth

SummaryThe liver possesses impressive regenerative capacities. Grafts of embryonic liver explants and liver explant-conditioned media have been shown to enhance the mitotic activity of hepatocytes. Hepatocyte growth factor (HGF), also named scatter factor (SF), has been identified as a primary candidate in promoting and regulating liver regeneration. Although initially thought to be a liver-specific mitogen, HGF was later reported to have mitogenic, motogenic, morphogenic, and anti-apoptotic activities in various cell types. By promoting angiogenesis and inhibiting apoptosis, endogenous HGF may play an important role in cardioprotection as well as in the regeneration of endothelial cells and cardiomyocytes after myocardial infarction. Since serum concentration of HGF increases in the early phase of myocardial infarction and in heart failure, HGF may also play a key role as a prognostic and diagnostic biomarker of cardiovascular disease. Here we discuss the role of HGF as a biomarker and mediator in cardioprotection and cardiovascular regeneration.

scholarly journals Emerging Role of Pericytes and Their Secretome in the Heart

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 548
Author(s):  
Han Su ◽  
Aubrey C. Cantrell ◽  
Heng Zeng ◽  
Shai-Hong Zhu ◽  
Jian-Xiong Chen
Keyword(s):  
Vascular Remodeling ◽  
Essential Role ◽  
Ischemic Heart Failure ◽  
Regenerative Processes ◽  
Angiogenic Growth Factors ◽  
Mural Cells ◽  
Cardiovascular Regeneration ◽  
The Brain ◽  
Lung And Kidney

Pericytes, as mural cells covering microvascular capillaries, play an essential role in vascular remodeling and maintaining vascular functions and blood flow. Pericytes are crucial participants in the physiological and pathological processes of cardiovascular disease. They actively interact with endothelial cells, vascular smooth muscle cells (VSMCs), fibroblasts, and other cells via the mechanisms involved in the secretome. The secretome of pericytes, along with diverse molecules including proinflammatory cytokines, angiogenic growth factors, and the extracellular matrix (ECM), has great impacts on the formation, stabilization, and remodeling of vasculature, as well as on regenerative processes. Emerging evidence also indicates that pericytes work as mesenchymal cells or progenitor cells in cardiovascular regeneration. Their capacity for differentiation also contributes to vascular remodeling in different ways. Previous studies primarily focused on the roles of pericytes in organs such as the brain, retina, lung, and kidney; very few studies have focused on pericytes in the heart. In this review, following a brief introduction of the origin and fundamental characteristics of pericytes, we focus on pericyte functions and mechanisms with respect to heart disease, ending with the promising use of cardiac pericytes in the treatment of ischemic heart failure.

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