Javascript must be enabled to continue!
The role of senescence in cancer therapy-associated cardiovascular toxicity
View through CrossRef
Cardiovascular diseases (CVDs) and cancer are the two leading causes of global mortality. Cancer treatments, including radiotherapy and chemotherapy, can have severe cardiotoxic side effects, raising concerns for cancer patients and increasing the financial burden on healthcare systems. Recent studies have shown a link between cancer therapy-induced cardiotoxicity and cardiac senescence. Specifically, systemic cancer therapies are known to induce cardiac senescence, which may directly result in cardiac dysfunction or enhance the vulnerability of the heart to other stressors. Besides anthracyclines, newer, more targeted therapies such as tyrosine kinase inhibitors (TKIs) have also been shown to induce cardiac senescence. Cellular senescence is triggered by DNA damage, oncogene activation, reactive oxygen and nitrogen species, and other stressors, leading to the secretion of proinflammatory factors, increased oxidative stress, and disruption of normal cellular functions. Understanding the molecular mechanisms of cardiac senescence induced by cancer therapy is essential for attenuating or even preventing clinically overt cardiotoxicity using senotherapies such as senolytics and senomorphics. In this review, cancer therapies that are associated with CVDs are described with an emphasis on the potential role of cardiac senescence in the disease progression. In addition, the known mechanisms by which anthracyclines, particularly doxorubicin (DOX), radiotherapy, and TKIs lead to cardiac senescence are highlighted. Finally, recent and novel senotherapies for treating cellular senescence are discussed with a focus on targeting cardiac senescence following cancer treatment. The field remains in its early stages, with further research required to clarify how cancer treatments contribute to cardiotoxicity. At the same time, identifying senotherapies that can be safely combined with cancer drugs is essential for targeting cardiac senescence and protecting cardiac health in cancer patients.
Title: The role of senescence in cancer therapy-associated cardiovascular toxicity
Description:
Cardiovascular diseases (CVDs) and cancer are the two leading causes of global mortality.
Cancer treatments, including radiotherapy and chemotherapy, can have severe cardiotoxic side effects, raising concerns for cancer patients and increasing the financial burden on healthcare systems.
Recent studies have shown a link between cancer therapy-induced cardiotoxicity and cardiac senescence.
Specifically, systemic cancer therapies are known to induce cardiac senescence, which may directly result in cardiac dysfunction or enhance the vulnerability of the heart to other stressors.
Besides anthracyclines, newer, more targeted therapies such as tyrosine kinase inhibitors (TKIs) have also been shown to induce cardiac senescence.
Cellular senescence is triggered by DNA damage, oncogene activation, reactive oxygen and nitrogen species, and other stressors, leading to the secretion of proinflammatory factors, increased oxidative stress, and disruption of normal cellular functions.
Understanding the molecular mechanisms of cardiac senescence induced by cancer therapy is essential for attenuating or even preventing clinically overt cardiotoxicity using senotherapies such as senolytics and senomorphics.
In this review, cancer therapies that are associated with CVDs are described with an emphasis on the potential role of cardiac senescence in the disease progression.
In addition, the known mechanisms by which anthracyclines, particularly doxorubicin (DOX), radiotherapy, and TKIs lead to cardiac senescence are highlighted.
Finally, recent and novel senotherapies for treating cellular senescence are discussed with a focus on targeting cardiac senescence following cancer treatment.
The field remains in its early stages, with further research required to clarify how cancer treatments contribute to cardiotoxicity.
At the same time, identifying senotherapies that can be safely combined with cancer drugs is essential for targeting cardiac senescence and protecting cardiac health in cancer patients.
Related Results
Abstract A16: Wnt antagonist SFRP1 functions as secreted mediator of senescence
Abstract A16: Wnt antagonist SFRP1 functions as secreted mediator of senescence
Abstract
The purpose of this study was 1) to identify the mediator(s) of senescence that are secreted from senescent cells and induce senescence in an autocrine and ...
Abstract 1850: Characterizing senescence response to PARP inhibition may provide opportunities for enhanced efficacy through combinations with senolytic agents
Abstract 1850: Characterizing senescence response to PARP inhibition may provide opportunities for enhanced efficacy through combinations with senolytic agents
Abstract
Background: Inhibition of poly (ADP-ribose) polymerase (PARP) is an exciting treatment strategy recently approved for prostate cancer patients with homologo...
Cometary Physics Laboratory: spectrophotometric experiments
Cometary Physics Laboratory: spectrophotometric experiments
<p><strong><span dir="ltr" role="presentation">1. Introduction</span></strong&...
Abstract 2842: 5-aza-2’-Deoxycytidine induces cellular senescence in non-small cell lung cancer
Abstract 2842: 5-aza-2’-Deoxycytidine induces cellular senescence in non-small cell lung cancer
Abstract
Background: Lung cancer is one of the refractory malignancies and the leading cause of cancer-related death worldwide. Although prognosis of lung cancer was...
Edoxaban and Cancer-Associated Venous Thromboembolism: A Meta-analysis of Clinical Trials
Edoxaban and Cancer-Associated Venous Thromboembolism: A Meta-analysis of Clinical Trials
Abstract
Introduction
Cancer patients face a venous thromboembolism (VTE) risk that is up to 50 times higher compared to individuals without cancer. In 2010, direct oral anticoagul...
Global spliceosome activity regulates entry into cellular senescence
Global spliceosome activity regulates entry into cellular senescence
Abstract
Cellular senescence is a state of permanent growth arrest that can ultimately contribute to aging. Senescence can be induced by various stressors and is ...
Fibroblast Senescence: A Risk Factor for Remodeling, Inflammation, and Arrhythmias in the Post‐MI Heart
Fibroblast Senescence: A Risk Factor for Remodeling, Inflammation, and Arrhythmias in the Post‐MI Heart
Objectives
Cellular senescence is a stress response involving permanent replicative arrest. It is accompanied by a complex senescence‐associated secretory pheno...
Identification of senescence markers on cultured human corneal endothelial cells
Identification of senescence markers on cultured human corneal endothelial cells
Aims/Purpose: Corneal transplantation is currently the most frequent type of transplantation globally. However, a chronic shortage of donor corneas makes traditional methods unsust...

