13 Juli 2025

Summary

Cell damage leads to cell death through two primary mechanisms: necrosis and apoptosis. Necrosis results from injury such as ischemia, toxins, or trauma, causing swelling, membrane rupture, and inflammation that damages surrounding tissue. Apoptosis, a regulated process, occurs due to DNA damage, protein misfolding, or infection and can be triggered by intrinsic or extrinsic pathways. Both pathways activate caspases, leading to DNA and protein degradation, but unlike necrosis, apoptosis avoids significant inflammation, with cell remnants cleared via phagocytosis.

Takeaways

• 😀 Necrosis and apoptosis are the two primary mechanisms of irreversible cell death.
• 😀 Necrosis occurs due to injury from ischemia, toxins, or trauma, disrupting ion balance and membrane integrity.
• 😀 Swelling of the cytoplasm and organelles, along with lysosomal enzyme leakage, are hallmarks of necrosis.
• 😀 In necrosis, denatured proteins cause hyper-eosinophilic cytoplasm, while DNA degradation leads to nuclear shrinkage and fragmentation.
• 😀 The disruption of the plasma membrane in necrosis results in leakage of cell contents into the extracellular space and inflammation.
• 😀 Inflammation from necrosis can cause further damage to surrounding tissues.
• 😀 Apoptosis is a more regulated form of cell death, which can occur due to DNA damage, protein misfolding, infection, or physiological processes.
• 😀 The intrinsic apoptosis pathway is triggered by damage or loss of survival signals, increasing pro-apoptotic factors like Bax and Bak.
• 😀 In apoptosis, the formation of mitochondrial pores releases cytochrome C, activating caspases and leading to cell degradation.
• 😀 The extrinsic apoptosis pathway is activated by external ligands binding to cell surface receptors, initiating caspase activation.
• 😀 Apoptotic cells undergo shrinkage, nuclear fragmentation, and cytoplasmic blebbing, while the cell membrane remains intact, avoiding significant inflammation.

Q & A

What are the two primary mechanisms of irreversible cell damage?

The two primary mechanisms of irreversible cell damage are necrosis and apoptosis.

What causes necrosis in cells?

Necrosis occurs due to cell injury from factors like ischemia, toxins, or trauma, which disrupt ion balance and membrane integrity.

What are the visible cellular changes associated with necrosis?

In necrosis, the cytoplasm and organelles swell, lysosomal enzymes leak and degrade cellular contents, and the DNA undergoes shrinkage, fragmentation, and disappearance of the nucleus.

How does necrosis affect the surrounding tissue?

Necrosis leads to leakage of cell contents into the extracellular space, triggering inflammation and recruitment of leukocytes, which can further damage nearby tissue.

How does apoptosis differ from necrosis?

Apoptosis is a regulated process that can occur physiologically or pathologically, unlike necrosis, which is typically unregulated and results from injury. Apoptosis does not cause significant inflammation.

What are the triggers for apoptosis?

Apoptosis can be triggered by DNA damage, protein misfolding, infection, and during normal physiological processes such as embryogenesis and hormone-driven events.

What is the intrinsic pathway of apoptosis?

The intrinsic pathway is activated when cell survival signals are lost or damaged, leading to the activation of pro-apoptotic factors and the formation of mitochondrial pores that release cytochrome C, activating caspases.

How does the extrinsic pathway of apoptosis work?

The extrinsic pathway is triggered when an external ligand binds to a receptor, initiating autocatalytic activation of caspases, which leads to cell death.

What are the results of both the intrinsic and extrinsic apoptosis pathways?

Both pathways lead to the activation of caspases, which degrade DNA and structural proteins, causing the cell to shrink, the nucleus to fragment, and the membrane to remain intact.

What happens to the remnants of apoptotic cells?

In apoptosis, the cell remnants are typically removed via phagocytosis, preventing significant inflammation in the surrounding tissue.