Intrinsic apoptosis

Definition

Intrinsic apoptosis is a form of programmed cell death that is initiated from within the cell, typically in response to internal stress signals such as DNA damage, oxidative stress, or loss of growth factors. This process is characterized by the release of cytochrome c from the mitochondria, leading to the activation of caspases that ultimately execute cell death. Intrinsic apoptosis plays a crucial role in maintaining cellular homeostasis and eliminating damaged or unwanted cells.

5 Must Know Facts For Your Next Test

1. Intrinsic apoptosis is primarily regulated by Bcl-2 family proteins, which determine whether a cell will undergo apoptosis based on various internal signals.
2. When a cell experiences significant stress, such as irreparable DNA damage, pro-apoptotic factors are released from the mitochondria, triggering the caspase cascade.
3. Cytochrome c release is a hallmark of intrinsic apoptosis and is essential for the activation of the apoptosome, which further activates caspases.
4. Intrinsic apoptosis is critical for development and tissue homeostasis, helping eliminate damaged cells and prevent tumor formation.
5. Disruption of intrinsic apoptosis pathways can lead to various diseases, including cancer, neurodegenerative disorders, and autoimmune diseases.

Review Questions

• How does the intrinsic apoptosis pathway differ from the extrinsic pathway of apoptosis?
  • The intrinsic apoptosis pathway is triggered by internal cellular stressors and involves mitochondrial changes leading to caspase activation, while the extrinsic pathway is initiated by external signals binding to death receptors on the cell surface. In intrinsic apoptosis, factors such as DNA damage or lack of survival signals prompt mitochondrial release of cytochrome c. In contrast, the extrinsic pathway relies on ligands like FasL binding to receptors that activate downstream signaling.
• Discuss the role of Bcl-2 family proteins in regulating intrinsic apoptosis and their implications in cancer biology.
  • Bcl-2 family proteins play a critical role in controlling intrinsic apoptosis by either promoting or inhibiting mitochondrial outer membrane permeabilization. Pro-apoptotic members like Bax and Bak promote cell death by facilitating cytochrome c release, whereas anti-apoptotic members like Bcl-2 prevent it. In cancer biology, overexpression of anti-apoptotic Bcl-2 proteins can allow cancer cells to evade apoptosis, contributing to tumor survival and resistance to therapies.
• Evaluate the significance of intrinsic apoptosis in cellular homeostasis and its potential impact on therapeutic strategies in cancer treatment.
  • Intrinsic apoptosis is essential for maintaining cellular homeostasis by removing damaged or dysfunctional cells that could lead to tumorigenesis. Understanding this process allows for targeted therapeutic strategies in cancer treatment, such as drugs that mimic pro-apoptotic signals or inhibit anti-apoptotic proteins. By restoring normal apoptotic pathways in cancer cells, therapies can potentially enhance cell death in tumors that are resistant to conventional treatments, thus improving patient outcomes.

Related terms

mitochondrial pathway: The pathway of intrinsic apoptosis that involves the mitochondria releasing pro-apoptotic factors, like cytochrome c, which activate caspases.

caspases: A family of cysteine proteases that are key mediators of apoptosis, responsible for cleaving specific substrates that lead to cellular breakdown during apoptosis.

Bcl-2 family proteins: A group of proteins that regulate intrinsic apoptosis by either promoting or inhibiting mitochondrial outer membrane permeabilization.