Apoptosis: Programmed Cell Death

Introduction

Apoptosis is a tightly regulated process of programmed cell death crucial for maintaining cellular homeostasis. It eliminates damaged, infected, or unnecessary cells through intrinsic and extrinsic pathways.

Intrinsic Pathway

The intrinsic pathway, also known as the mitochondrial pathway, is initiated by internal cellular stressors such as DNA damage or oxidative stress. This leads to mitochondrial outer membrane permeabilization (MOMP), releasing cytochrome c, which activates apoptosome formation and caspase cascade.

• Key Regulators: Bcl-2 family proteins (pro-apoptotic Bax, Bak; anti-apoptotic Bcl-2, Bcl-xL)
• Execution Mechanism: Caspase-9 activation leading to downstream caspase-3 and caspase-7 activation

Extrinsic Pathway

The extrinsic pathway is initiated by extracellular death signals binding to cell surface receptors such as TNF receptor or Fas ligand. This interaction leads to the formation of the death-inducing signaling complex (DISC), which activates caspase-8 and caspase-10.

• Key Regulators: Death receptors (Fas/CD95, TNFR1)
• Execution Mechanism: Caspase-8 activation leading to caspase-3 activation

Apoptosis vs. Necrosis

Unlike necrosis, apoptosis is a controlled, energy-dependent process that prevents inflammation. It is essential for embryogenesis, immune response modulation, and cancer prevention.

Conclusion

Understanding apoptosis pathways is pivotal for advancing treatments related to cancer, neurodegenerative disorders, and autoimmune diseases. Targeting apoptosis mechanisms offers promising therapeutic potential.