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1kits（10Vials）
▎Cardiogen Structure
Source: PubChem | Sequence: AEDR Molecular Formula: C18H31N7O9 Molecular Weight: 489.5 g/mol PubChem CID：11583989 Synonyms: SCHEMBL3194515 |
▎Cardiogen Research
What is the research background of Cardiogen?
Driven by the needs of tumor prevention/treatment and cardiovascular disease therapy, research on Cardiogen has garnered significant attention. Researchers have found that Cardiogen peptide inhibits transplantable M-1 sarcoma, inducing tumor cell apoptosis and hemorrhagic necrosis, providing a new direction for tumor treatment. Meanwhile, its potential value in regulating cardiac physiological indices and promoting myocardial regeneration has also brought new opportunities for cardiovascular disease treatment research.
With the rise of bioactive peptide drug development, the study of Cardiogen’s structure and function is of great significance as a biologically active peptide with unique properties. The development of technologies such as genetic engineering and proteomics has provided technical support for in-depth exploration of Cardiogen’s origin and clarification of its mechanism of action, driving related research forward.
What is the mechanism of action of Cardiogen?
Induction of Tumor Cell Apoptosis: Studies show that after injecting Cardiogen into rats with transplantable M-1 sarcoma, the level of tumor cell apoptosis in all experimental groups was higher than that in the control group. This indicates that Cardiogen can trigger apoptosis mechanisms within tumor cells through certain pathways, prompting tumor cells to undergo programmed cell death. Apoptosis is a process in which cells actively end their lives following their own programs under certain physiological or pathological conditions. Normally, apoptosis is precisely regulated by a series of genes and signaling pathways. Cardiogen may activate apoptosis-related genes or signaling pathways, such as acting on Bcl-2 family proteins to increase the expression of pro-apoptotic proteins (e.g., Bax) or inhibit the function of anti-apoptotic proteins (e.g., Bcl-2), thereby inducing the release of cytochrome C from mitochondria into the cytoplasm and activating the caspase cascade reaction, ultimately leading to tumor cell apoptosis[1] .
Figure 1. Epigenetic mechanisms in cardiovascular disorders. The heart (center) connects to three major epigenetic regulatory mechanisms influencing cardiovascular pathophysiology.
Source:MDPI[5]
Induction of Tumor Hemorrhagic Necrosis: The dose-dependent inhibition of M-1 sarcoma growth after Cardiogen injection is partially due to tumor hemorrhagic necrosis. Tumor growth relies on neovascularization for nutrients and oxygen. Cardiogen may achieve this effect by affecting the normal function of the tumor vascular network. It may act on tumor vascular endothelial cells, interfering with the signaling of angiogenesis-related factors (such as vascular endothelial growth factor VEGF), disrupting the proliferation, migration, and lumen formation capabilities of vascular endothelial cells, leading to impaired tumor angiogenesis, local ischemia, and hypoxia in tumor tissues, and inducing hemorrhagic necrosis. At the same time, it may directly damage existing tumor blood vessels, causing vascular rupture and bleeding, further exacerbating tumor tissue necrosis [1].
Non-Direct Cytostatic Effect: From the perspective of proliferation activity parameters, tumor growth inhibition is not caused by the direct cytostatic effect of Cardiogen on tumor cells. This means it does not directly inhibit basic metabolic processes such as tumor cell DNA synthesis or protein synthesis like traditional cytotoxic drugs to prevent tumor cell proliferation. Instead, it inhibits tumor growth through indirect mechanisms such as inducing apoptosis and causing tumor hemorrhagic necrosis. This characteristic of non-direct cytostatic action may make Cardiogen potentially safer with relatively low toxicity to normal cells while exerting anti-tumor effects [1].
Action Through Tumor Vascular Network: Morphological evidence suggests that Cardiogen’s action involves a specific mechanism through the tumor vascular network. The tumor vascular network not only provides nutrients for tumor cells but also plays a key role in tumor metastasis and other processes. Cardiogen may bind to specific receptors on the surface of cells (such as endothelial cells and pericytes) in the tumor vascular network, activating intracellular signal transduction pathways and triggering a series of biological effects, such as regulating vascular permeability and influencing the contraction and relaxation of vascular smooth muscle cells, thereby affecting the tumor tissue microenvironment and ultimately influencing tumor growth, apoptosis, and other processes.
Additionally, the abnormal structure and function of the tumor vascular network provide a basis for Cardiogen’s targeted action, enabling it to act relatively specifically on tumor tissues with minimal impact on normal tissue blood vessels[1]
What are the applications of Cardiogen?
Effects on Cardiac-Related Indices: Under stress conditions, Cardiogen plays an important role in regulating heart rate and organ weight parameters in rats. Studies have shown that Cardiogen injection can compensate for the stress-induced effects of adrenaline on the relative mass changes of the heart, adrenal glands, and spleen, normalizing the relative masses of these organs. At the same time, it helps reduce heart rate to control values and alleviate the manifestations of arrhythmia under stress. This indicates that Cardiogen can maintain the normal physiological state of the heart and related organs in stressful environments, positively contributing to stabilizing the cardiovascular system[2].
Applications in the Treatment of Heart Diseases
Myocardial Infarction Treatment: Cardiogenin, an active component isolated from plant extracts (possibly related to Cardiogen or one of its active ingredients), has demonstrated significant efficacy in animal models of myocardial infarction. Studies have found that cardiogenin can significantly repair infarcted hearts, with endogenous mesenchymal stem cells (MSCs) observed to differentiate into new cardiomyocytes in the infarcted area, accompanied by significant improvement in cardiac function.
Transplanting MSCs pre-treated with EGJ (a plant extract containing cardiogenin) or cardiogenin into myocardial infarction animal models also promotes substantial regeneration of functional myocardium. This indicates that cardiogenin not only has the ability to promote myocardial regeneration but can also activate MSCs, providing necessary conditions for myocardial regeneration and opening new avenues for myocardial infarction treatment. Furthermore, oral administration of cardiogenin has also been shown to have significant therapeutic effects on myocardial infarction, with bone marrow-derived endogenous MSCs confirmed as the primary cell source for regenerated myocardium. Preliminary mechanistic studies suggest that miR-9 and its target E-cadherin may be involved in the formation of intercalated discs[3, 4].
Applications in Cancer Treatment: Cardiogen peptide exhibits tumor-modifying effects in rats with transplanted M-1 sarcoma. Studies have shown that after Cardiogen injection, the level of tumor cell apoptosis in all experimental groups was higher than that in the control group, and the drug inhibited M-1 sarcoma growth in a dose-dependent manner. This inhibitory effect does not stem from the drug’s direct cytostatic action on tumors but rather from inducing tumor hemorrhagic necrosis and stimulating tumor cell apoptosis. Morphologically, Cardiogen may exert its specific mechanism of action through the tumor vascular network, providing a new potential strategy for cancer treatment by regulating the tumor microenvironment and inducing tumor cell apoptosis [3, 4].
Conclusion
In summary, Cardiogen can regulate the cardiovascular system, improve the function of the heart and related organs under stress, and promote myocardial infarction repair. Meanwhile, its peptide form can induce tumor cell apoptosis, cause hemorrhagic necrosis, and inhibit tumor growth, providing new directions for disease treatment.
About The Author
The above-mentioned materials are all researched, edited and compiled by Cocer Peptides.
Scientific Journal Author
Cheng, Lei is a distinguished scholar with extensive research experience in life sciences and materials science. Affiliated with prestigious institutions such as Hong Kong Polytechnic University, Dali University, and Chinese University of Hong Kong, he has demonstrated a diverse and in-depth academic background. His research spans across Biochemistry & Molecular Biology, Cell Biology, and Materials Science, which are at the forefront of modern scientific research and hold significant application potential. Cheng, Lei's work focuses not only on fundamental scientific exploration but also on the integration of science and technology, providing robust support for theoretical development and technological innovation in related fields. His collaborative efforts with various academic institutions have also been instrumental in promoting academic exchange and research cooperation.. Cheng, Lei is listed in the reference of citation [3].
