Therapy-induced senescence through the redox lens.

Area of Science:

• Oncology
• Cellular Biology
• Biochemistry

Background:

• Therapy-induced senescent tumor cells contribute to tumor recurrence and relapse.
• Reactive oxygen species (ROS) and redox signaling are critical in initiating and establishing therapy-induced senescence.
• Senescent cells release factors (SASP) that impact the tumor microenvironment.

Purpose of the Study:

• To review the role of ROS and redox dynamics in therapy-induced senescence.
• To explore the link between ROS, inflammation, and SASP production.
• To discuss senotherapeutic strategies targeting redox pathways and potential implications of redox rewiring.

Main Methods:

• Literature review focusing on ROS, redox signaling, and therapy-induced senescence.
• Analysis of the interplay between oxidative stress, cellular senescence, and the tumor microenvironment.
• Evaluation of potential interventional strategies, including senotherapeutics.

Main Results:

• Excess ROS can cause oxidative DNA damage, leading to cellular senescence.
• Redox state dynamics influence cellular fate towards senescence and SASP production.
• Redox rewiring may play a role in escaping therapy-induced senescence.

Conclusions:

• Understanding redox-driven mechanisms in therapy-induced senescence is crucial for combating tumor recurrence.
• Modulating redox and antioxidant pathways offers potential senotherapeutic targets.
• Integrating multi-omics approaches with redox analysis can elucidate senescence heterogeneity and inform novel treatment strategies.