negative regulation of cardiac muscle cell apoptotic process

Definition

Target type: biologicalprocess

Any process that decreases the rate or extent of cardiac cell apoptotic process, a form of programmed cell death induced by external or internal signals that trigger the activity of proteolytic caspases whose actions dismantle a cardiac muscle cell and result in its death. [GOC:BHF, GOC:dph, GOC:mtg_apoptosis, GOC:rl, GOC:tb]

Negative regulation of cardiac muscle cell apoptotic process involves a complex interplay of signaling pathways that suppress programmed cell death in cardiomyocytes, preventing heart damage and maintaining cardiac function. This process is essential for the survival and repair of the heart, ensuring its proper functioning under physiological and pathological conditions.

Key players in this process include:

1. **Anti-apoptotic signaling pathways**: These pathways activate pro-survival genes and proteins that counteract the apoptotic cascade. Examples include:
* **PI3K/Akt pathway**: This pathway is activated by growth factors and other survival signals. Akt phosphorylates and inhibits pro-apoptotic proteins like Bad and caspase-9, promoting cell survival.
* **MAPK/ERK pathway**: This pathway is activated by growth factors and stress signals. ERK phosphorylates and activates transcription factors like Elk-1 and c-Fos, which promote the expression of anti-apoptotic genes.
* **NF-κB pathway**: This pathway is activated by stress signals and cytokines. NF-κB translocates to the nucleus and activates the expression of anti-apoptotic genes like IAPs (inhibitors of apoptosis proteins) and Bcl-2.

2. **Anti-apoptotic proteins**: These proteins directly inhibit the apoptotic machinery. Examples include:
* **Bcl-2 family**: These proteins include both pro-apoptotic (e.g., Bax, Bak) and anti-apoptotic (e.g., Bcl-2, Bcl-xL) members. Anti-apoptotic Bcl-2 proteins bind to pro-apoptotic members, preventing the formation of the mitochondrial permeability transition pore (MPTP) and cytochrome c release.
* **IAPs**: These proteins directly bind to and inhibit caspases, the executioner enzymes of apoptosis.

3. **Chaperones**: These proteins help maintain protein homeostasis and prevent misfolded proteins from triggering apoptosis. Examples include:
* **Hsp70**: This chaperone binds to unfolded proteins, promoting their refolding and preventing their aggregation.
* **Hsp90**: This chaperone interacts with various signaling proteins, ensuring their proper folding and function.

4. **Autophagy**: This process involves the degradation of cellular components, providing building blocks for cell survival and removing damaged organelles. Autophagy is essential for heart function and can protect cardiomyocytes from apoptosis.

The interplay between these pathways and proteins creates a sophisticated network that ensures cardiac muscle cell survival. Disruption of these pathways can lead to cardiomyocyte apoptosis and heart disease. For instance, in heart failure, the balance between pro- and anti-apoptotic signaling is disrupted, leading to increased apoptosis and cardiac dysfunction.'
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Proteins (6)

Compounds (263)