positive regulation of cell growth involved in cardiac muscle cell development
Definition
Target type: biologicalprocess
Any process that increases the rate, frequency, or extent of the growth of a cardiac muscle cell, where growth contributes to the progression of the cell over time from its initial formation to its mature state. [GOC:dph]
Positive regulation of cell growth involved in cardiac muscle cell development is a complex and tightly regulated process that ensures the proper formation and function of the heart. It involves the coordinated action of a variety of signaling pathways, transcription factors, and growth factors.
**Key Steps:**
1. **Signal transduction:** The process begins with the activation of signaling pathways, such as the MAPK/ERK, PI3K/AKT, and TGF-beta pathways, in response to external stimuli. These stimuli can include growth factors like fibroblast growth factor (FGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF), as well as mechanical cues.
2. **Transcriptional regulation:** Activated signaling pathways converge on transcription factors, such as MEF2, GATA4, and NKX2.5, which regulate the expression of genes involved in cell cycle progression, protein synthesis, and cell survival.
3. **Cell cycle control:** Transcription factors and signaling pathways interact to promote the expression of cyclins and cyclin-dependent kinases (CDKs), which are crucial for the progression through different phases of the cell cycle.
4. **Protein synthesis and differentiation:** During cardiac muscle cell development, the expression of sarcomeric proteins, including actin, myosin, and troponin, is increased. These proteins are essential for the contractile function of the heart.
5. **Cell survival and apoptosis:** Positive regulation of cell growth also involves the suppression of apoptosis, a programmed cell death pathway that eliminates unnecessary or damaged cells.
**Molecular Mechanisms:**
* **Growth factors and their receptors:** Growth factors bind to their receptors, activating downstream signaling pathways, leading to the phosphorylation and activation of transcription factors.
* **Signaling pathways:** These pathways, such as MAPK/ERK and PI3K/AKT, promote cell survival, proliferation, and differentiation through the activation of specific target proteins.
* **Transcription factors:** Transcription factors bind to specific DNA sequences, regulating the expression of genes involved in cell growth and development.
* **MicroRNAs (miRNAs):** These small non-coding RNAs can fine-tune gene expression by targeting specific mRNAs, affecting cell growth and differentiation.
**Clinical Implications:**
Dysregulation of positive regulation of cell growth during cardiac muscle cell development can lead to various heart defects, including congenital heart disease and cardiomyopathies. Understanding this intricate process is crucial for developing therapeutic strategies to treat these conditions.'
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Proteins (1)
| Protein | Definition | Taxonomy |
|---|---|---|
| Poly [ADP-ribose] polymerase 2 | A poly [ADP-ribose] polymerase 2 that is encoded in the genome of human. [PRO:DNx] | Homo sapiens (human) |
Compounds (14)
| Compound | Definition | Classes | Roles |
|---|---|---|---|
| pj-34 | PJ34 : A member of the class of phenanthridines that is 5,6-dihydrophenanthridine substituted at positions 2 and 6 by (N,N-dimethylglycyl)amino and oxo groups, respectively. It is a potent inhibitor of poly(ADP-ribose) polymerases PARP1 and PARP2 (IC50 of 110 nM and 86 nM, respectively) and exhibits anti-cancer, cardioprotective and neuroprotective properties. | phenanthridines; secondary carboxamide; tertiary amino compound | angiogenesis inhibitor; anti-inflammatory agent; antiatherosclerotic agent; antineoplastic agent; apoptosis inducer; cardioprotective agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; neuroprotective agent |
| 4-Methoxybenzamide | benzamides | ||
| amentoflavone | biflavonoid; hydroxyflavone; ring assembly | angiogenesis inhibitor; antiviral agent; cathepsin B inhibitor; P450 inhibitor; plant metabolite | |
| rucaparib | AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source | azepinoindole; caprolactams; organofluorine compound; secondary amino compound | antineoplastic agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor |
| veliparib | benzimidazoles | EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor | |
| olaparib | cyclopropanes; monofluorobenzenes; N-acylpiperazine; phthalazines | antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor | |
| niraparib | 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide : A member of the class of indazoles that is 2H-indazole substituted by 4-(piperidin-3-yl)phenyl and aminocarbonyl groups at positions 2 and 7, respectively. It is a potent PARP1 inhibitor with IC50 of 3.2 nM. | benzenes; indazoles; piperidines; primary carboxamide | antineoplastic agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor |
| niraparib | niraparib : A 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide that has S-configuration. It is a potent inhibitor of PARP1 and PARP2 (IC50 of 3.8 and 2.1 nM, respectively) and approved as a first-line maintenance treatment for women with advanced ovarian cancer after responding to platinum-based chemotherapy. niraparib: structure in first source | 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide | antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; radiosensitizing agent |
| iwr-1 endo | IWR-1-endo : A dicarboximide having an endo bridged phthalimide structure, substituted at nitrogen by a 4-(quinolin-8-ylcarbamoyl)benzoyl group. | benzamides; bridged compound; dicarboximide; quinolines | axin stabilizer; Wnt signalling inhibitor |
| nms-p118 | NMS-P118: a PARP-1 inhibitor; structure in first source | ||
| g007-lk | G007-LK: potent and specific small-molecule tankyrase inhibitor; structure in first source | ||
| xav939 | XAV939 : A thiopyranopyrimidine in which a 7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidine skeleton is substituted at C-4 by a hydroxy group and at C-2 by a para-(trifluoromethyl)phenyl group. XAV939: selectively inhibits beta-catenin-mediated transcription; structure in first source | (trifluoromethyl)benzenes; thiopyranopyrimidine | tankyrase inhibitor |
| bmn 673 | talazoparib: inhibits both PARP1 and PARP2; structure in first source | ||
| nvp-tnks656 |