Oxidative stress is presented as the consequence of disrupted redox balance and as a dominant factor across multiple phases of cancer. The review uses it to connect tumour biology with host immune dysfunction.
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oxidative stress
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Cellular senescence and oxidative stress constitute an interdependent axis that underlies cardiac pathophysiology.
Any deregulation of this subtle balance can result in oxidative stress that can lead to various pathological conditions including cancer. Oxidative stress can be a cause of neoplasia, or it can be induced by a growing tumour itself.
Free radicals can adversely affect various important classes of biological molecules such as nucleic acids, lipids, and proteins, thereby altering the normal redox status leading to increased oxidative stress.
Oxidative stress is a condition of imbalance between reactive oxygen species formation and cellular antioxidant capacity due to enhanced ROS generation and/or dysfunction of the antioxidant system.
Broad aging reviews discovered in PubMed treat oxidative stress as the main mechanistic process linking free radicals to aging.
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Linked Claims
In the heart, cellular senescence and oxidative stress influence remodeling and dysfunction across ischemia-reperfusion injury, heart failure with preserved ejection fraction, dilated cardiomyopathy, and cardiac hypertrophy.
Quoted textsource-backed
In the heart, cellular senescence and oxidative stress influence remodeling and dysfunction across diseases, including ischemia-reperfusion injury, heart failure with preserved ejection fraction, dilated cardiomyopathy, and cardiac hypertrophy.
Cellular senescence and oxidative stress form an interdependent axis underlying cardiac pathophysiology.
Quoted textsource-backed
Cellular senescence and oxidative stress constitute an interdependent axis that underlies cardiac pathophysiology.
Cellular senescence is initiated and sustained by redox imbalance.
Quoted textsource-backed
Cellular senescence, defined as durable proliferative arrest, is initiated and sustained by redox imbalance
The article provides an overview of mechanisms and functions of cellular senescence in response to oxidative stress and redox signaling in cardiac disease and integrates experimental and clinical evidence to discuss mechanism-informed prevention and therapy.
Quoted textsource-backed
In this review, we attempt to provide an overview of the fundamental mechanisms and functions of cellular senescence in response to oxidative stress and redox signaling in disease. In addition, we integrate experimental and clinical evidence and delineate implications for mechanism-informed prevention and therapy.
Oxidative stress can contribute to cancer and can also be induced by a growing tumour.
In tumour-bearing hosts, direct oxidative stress from tumour cells and oxidative stress mediators in the tumour microenvironment contribute to suppression of effector T cell function and induction of T cell death.
Reactive oxygen species are normal signaling mediators but, when not tightly balanced by antioxidant and enzyme systems, can drive oxidative stress that damages cellular components.
The review presents oxidative stress as a dominant factor across cancer initiation, progression, and establishment, within tumour-stroma-immune system interactions.
Free-radical-induced oxidative stress has been reported to be involved in diabetes mellitus, neurodegenerative disorders, cardiovascular diseases, asthma, cataract development, rheumatoid arthritis, and multiple cancers.
Quoted textsource-backed
The free radicals induced oxidative stress has been reported to be involved in several diseased conditions such as diabetes mellitus, neurodegenerative disorders (Parkinson's disease-PD, Alzheimer's disease-AD and Multiple sclerosis-MS), cardiovascular diseases (atherosclerosis and hypertension), respiratory diseases (asthma), cataract development, rheumatoid arthritis and in various cancers (colorectal, prostate, breast, lung, bladder cancers).
Free radicals can damage nucleic acids, lipids, and proteins, altering redox status and increasing oxidative stress.
Quoted textsource-backed
Free radicals can adversely affect various important classes of biological molecules such as nucleic acids, lipids, and proteins, thereby altering the normal redox status leading to increased oxidative stress.
Oxidative stress is defined as an imbalance between reactive oxygen species formation and cellular antioxidant capacity caused by increased ROS generation and/or antioxidant system dysfunction.
Quoted textsource-backed
Oxidative stress is a condition of imbalance between reactive oxygen species formation and cellular antioxidant capacity due to enhanced ROS generation and/or dysfunction of the antioxidant system.
Biochemical alterations in macromolecules affected by oxidative stress can contribute to pathological conditions and are especially linked to neurodegenerative diseases.
Quoted textsource-backed
Biochemical alterations in these macromolecular components can lead to various pathological conditions and human diseases, especially neurodegenerative diseases.
Deposition of abnormal aggregated proteins and disruption of metal ion homeostasis are highly associated with oxidative stress in neurodegenerative disease context.
Quoted textsource-backed
Deposition of abnormal aggregated proteins and disruption of metal ions homeostasis are highly associated with oxidative stress.