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Intracellular second messengers mediate stress inducible hormesis and Programmed Cell Death: A review
David R Zhou1, Rawan Eid1, Katie A Miller2
1Department of Chemistry and Chemical Engineering, Royal Military College, Kingston, Ontario, Canada; Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada.
Cellular stress triggers numerous second messengers, not just Reactive Oxygen Species (ROS). Understanding these diverse signaling molecules is key to deciphering cell survival and death pathways.
Area of Science:
- Cellular biology
- Biochemistry
- Stress response pathways
Background:
- Cellular stress induces a wide array of responses, including apoptosis and hormesis.
- Second messenger systems play a critical role in mediating these stress responses.
- Current research often overemphasizes classical mediators like Reactive Oxygen Species (ROS), calcium, and ceramide, neglecting others.
Purpose of the Study:
- To review the diverse intracellular second messengers involved in cellular stress responses.
- To emphasize the multifaceted nature of initial stress-mediated signaling.
- To highlight the potential of studying second messenger systems for understanding stress-induced programmed cell death (PCD).
Main Methods:
- Literature review of intracellular second messengers in stress responses.
- Integration of information on diverse second messenger systems.
- Analysis of the role of second messengers in initiating cell survival and death pathways.
Main Results:
- Cellular stress activates a multitude of intracellular second messengers simultaneously.
- These diverse second messengers collectively orchestrate cell survival and/or cell death outcomes.
- The complexity of second messenger networks is often underestimated.
Conclusions:
- Initial cellular responses to stress involve a broad spectrum of second messengers.
- A comprehensive understanding of these signaling networks is crucial for elucidating stress-mediated PCD.
- Further investigation into various second messenger systems can illuminate the initiation of stress-induced cell death.
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