Target type: biologicalprocess
Any apoptotic process that contributes to the shaping of an endocardial cushion. The endocardial cushion is a specialized region of mesenchymal cells that will give rise to the heart septa and valves. [GOC:mtg_apoptosis, GOC:mtg_heart]
Apoptosis, a tightly regulated process of programmed cell death, plays a crucial role in the formation of the endocardial cushions, the precursors of heart valves and septa. The endocardial cushions arise from the endocardium, the inner lining of the heart, and undergo significant cellular remodeling during development. This remodeling involves the migration, proliferation, and programmed death of endocardial cells.
Apoptosis is initiated by signaling cascades that activate a cascade of caspases, a family of cysteine proteases. Caspases dismantle the cell in a controlled manner, breaking down its structural components and DNA. This process is essential for the proper shaping and remodeling of the endocardial cushions.
Several factors trigger apoptosis in the endocardial cushions, including:
* **Transforming growth factor-beta (TGF-beta) family signaling:** TGF-beta signaling, a major regulator of endocardial cushion development, induces apoptosis in specific regions of the endocardium.
* **Bone morphogenetic protein (BMP) signaling:** BMPs, a subgroup of TGF-beta family members, also contribute to apoptosis in the endocardial cushions, influencing the formation of valve leaflets and septa.
* **Fibroblast growth factor (FGF) signaling:** FGFs, involved in various developmental processes, can promote apoptosis in the endocardium, contributing to the precise shaping of the cushions.
* **Other signaling pathways:** Other signaling pathways, such as the Notch and Wnt pathways, also play roles in regulating apoptosis during endocardial cushion development.
Apoptosis ensures the proper removal of cells that are no longer needed, allowing for the formation of the intricate structures of the heart valves and septa. The precise regulation of apoptosis is crucial for normal heart development, and dysregulation can lead to congenital heart defects.
Furthermore, the apoptotic process facilitates the formation of the endocardial cushions by:
* **Creating space for cell migration:** Apoptosis clears out cells in specific regions, allowing for the migration of other cells into these areas.
* **Promoting cell differentiation:** Apoptosis triggers signaling cascades that promote the differentiation of surviving cells into specialized cell types that form the heart valves and septa.
In conclusion, apoptosis is a fundamental process in endocardial cushion morphogenesis, ensuring the proper shaping and remodeling of these structures. It is tightly regulated by a complex network of signaling pathways, and its disruption can lead to serious heart defects.'
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| Protein | Definition | Taxonomy |
|---|---|---|
| Bone morphogenetic protein 4 | A bone morphogenetic protein 4 that is encoded in the genome of human. [PRO:CNA, UniProtKB:P12644] | Homo sapiens (human) |
| Compound | Definition | Classes | Roles |
|---|---|---|---|
| dorsomorphin | dorsomorphin : A pyrazolopyrimidine that is pyrazolo[1,5-a]pyrimidine which is substituted at positions 3 and 6 by pyridin-4-yl and p-[2-(piperidin-1-yl)ethoxy]phenyl groups, respectively. It is a potent, selective, reversible, and ATP-competitive inhibitor of AMPK (AMP-activated protein kinase, EC 2.7.11.31) and a selective inhibitor of bone morphogenetic protein (BMP) signaling. dorsomorphin: an AMPK inhibitor | aromatic ether; piperidines; pyrazolopyrimidine; pyridines | bone morphogenetic protein receptor antagonist; EC 2.7.11.31 {[hydroxymethylglutaryl-CoA reductase (NADPH)] kinase} inhibitor |
| ldn 193189 | LDN 193189: inhibits bone morphogenetic protein signaling | pyrimidines | |
| ml347 | ML347: an ALK2 inhibitor; structure in first source |