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cellular senescence

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Evidence Snippets

Cellular senescence and oxidative stress constitute an interdependent axis that underlies cardiac pathophysiology.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1disease associationsupports2025Source 1DOIPubMed

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.
Claim 2mechanistic relationshipsupports2025Source 1DOIPubMed

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.
Claim 3mechanistic relationshipsupports2025Source 1DOIPubMed

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
Claim 4review scopesupports2025Source 1DOIPubMed

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.