Cardiogen Peptide Research in Cardiac Function and Damaged Tissue

Cardiogen is a short peptide characterized as a bioregulator with distinctive properties centered around fibroblasts, cells considered responsible for tissue repair and scar formation. Although initially studied for its involvement in various cardiovascular diseases, studies suggest Cardiogen’s impact extends beyond the cardiovascular system, showcasing potential impact in diverse tissues. 

Research has suggested that Cardiogen may host synergistic properties, augmenting the efficacy of conventional compounds and thereby possibly enhancing long-term. Furthermore, early investigations on rat models indicate that Cardiogen may stimulate apoptosis in tumor cells, presenting a potential avenue for future exploration. These findings collectively emphasize the multifaceted potential of Cardiogen and its promising role in modulating cellular activities, fostering tissue repair, and potentially influencing tumorigenic processes.

Research indicates that Cardiogen peptide may influence fibroblast behavior by promoting the synthesis and secretion of specific extracellular matrix components, such as collagen and elastin, which are considered essential for tissue integrity and regeneration. Additionally, Cardiogen has been suggested to stimulate the proliferation of fibroblasts, facilitating the formation of new tissue and aiding in the healing process.⁽¹⁾

Studies also indicate that Cardiogen may stimulate the proliferation and differentiation of cardiac progenitor cells, which may generate new cardiac muscle cells. By facilitating the regeneration of damaged or diseased myocardium, Cardiogen peptide may potentially restore cardiac function.

 

Research Studies on the Cardiogen Peptide

Cardiogen and Cardiac System

Scientific investigation suggests that Cardiogen peptide may potentially induce cardiomyocyte proliferation while possibly suppressing fibroblast proliferation and maturation. This dual action might culminate in diminished scar formation and favorable long-term outcomes pertaining to cardiac remodeling, ultimately mitigating the progression toward heart failure. Furthermore, emerging data suggests that Cardiogen peptide may exert an inhibitory action on p53 protein expression, attenuating apoptotic rates.⁽²⁾

As per the researchers, “the tetrapeptide cardiogen demonstrated the great stimulating effect on the proliferation both in tissues from young and old rats. The immunohistochemical study demonstrated a decrease of the p53 protein expression by cardiogen action. This fact can testify that cardiogen inhibits the apoptosis process in the myocardial tissue.”⁽²⁾

Cardiogen Peptide and Prostate Cance

In vitro studies have suggested that Cardiogen, along with a group of related peptides, may exert potential regulatory action on the expression of signaling factors in prostate fibroblasts. These signaling factors are considered crucial in establishing a favorable microenvironment within tumors and are implicated in the development and progression of prostate cancer. 

Scientific data suggests aging and senescent fibroblasts can exhibit significant alterations in the synthesis of these signaling factors, potentially elucidating the higher incidence of prostate cancer in older individuals compared to younger counterparts. Remarkably, compelling evidence suggests that Cardiogen may restore the levels of these signaling molecules to levels comparable to, or even surpassing, those observed in youthful cell cultures.⁽³⁾

As per O V Kheifets et al., “These studies show promise for detailed development of methods of peptides’ regulation of aging and age-correction of violations of functioning of the prostate gland.”⁽⁴⁾

Cardiogen Peptide and Tumor Growth

Studies suggest that the Cardiogen peptide may exhibit contrasting action on apoptosis regulation in different cell types. Researchers posit that while it may reduce apoptosis in cardiac cells by down-regulating p53 expression, emerging data from rat models of M-1 sarcoma suggests that Cardiogen may lead to heightened levels of apoptosis in tumor cells.⁽⁵⁾ Moreover, the concentration-dependent nature of this action underscores its possible biological relevance.

Drs. Levdik and Knyazkin, esteemed researchers affiliated with the St. Petersburg Institute of Bioregulation and Gerontology and the Russian Academy of Medical Sciences, have extensively investigated the influence of amino acids and short peptides on both cancerous and pre-cancerous tissues. Their research endeavors involved studying the “tumor-modifying effect of cardiogen peptide on rats with transplanted M-1 sarcoma.” As per the results, “the level of apoptosis of tumor cells after cardiogen injections in all experimental groups was higher than in the control. The dose-dependent inhibition of M-1 sarcoma growth after injection of cardiogen was caused by the development of hemorrhagic necrosis and stimulation of tumor cell apoptosis.”⁽⁵⁾

 

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References:

1. Khavinson VK, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules. 2021 Nov 22;26(22):7053. doi: 10.3390/molecules26227053. PMID: 34834147; PMCID: PMC8619776. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8619776/ 
2. Chalisova NI, Lesniak VV, Balykina NA, Urt’eva SA, Urt’eva TA, Sukhonos IuA, Zhekalov AN. [The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats]. Adv Gerontol. 2009;22(3):409-13. Russian. PMID: 20210190. https://pubmed.ncbi.nlm.nih.gov/20210190/ 
3. Begley L, Monteleon C, Shah RB, Macdonald JW, Macoska JA. CXCL12 overexpression and secretion by aging fibroblasts enhance human prostate epithelial proliferation in vitro. Aging Cell. 2005 Dec;4(6):291-8. doi: 10.1111/j.1474-9726.2005.00173.x. PMID: 16300481. https://pubmed.ncbi.nlm.nih.gov/16300481/ 
4. Kheĭfets OV, Poliakova VO, Kvetnoĭ IM. [Peptidergic regulation of the expression of signal factors of fibroblast differentiation in the human prostate gland in cell aging]. Adv Gerontol. 2010;23(1):68-70. Russian. PMID: 20586252. https://pubmed.ncbi.nlm.nih.gov/20586252/ 
5. Levdik NV, Knyazkin IV. Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent rats. Bull Exp Biol Med. 2009 Sep;148(3):433-6. English, Russian. doi: 10.1007/s10517-010-0730-9. PMID: 20396706. https://pubmed.ncbi.nlm.nih.gov/20396706/ 
6. Image source: National Center for Biotechnology Information (2023). PubChem Compound Summary for CID 11583989, H-Ala-Glu-Asp-Arg-OH. Retrieved May 24, 2023 from https://pubchem.ncbi.nlm.nih.gov/compound/H-Ala-Glu-Asp-Arg-OH.