Mitochondria are considered to play complex roles in energy production, cellular signaling, and metabolism, serving as the cell’s powerhouse. Earlier assumptions about the control of mitochondria’s function, maintenance, and biogenesis by the nucleus may be reconsidered in light of newer studies suggesting that some mitochondria possess a genomic sequence, translating into proteins that may affect the genomic expression of the nucleus.

Research on the genomic sequence of mitochondria suggests that the rRNA possesses Open Reading Frames (ORFs), transcribing into small peptides, including Humanin (HN), Small Humanin-Like Peptides 1-6 (SHLPs), and Mitochondrial ORF-encoded peptide (MOTS-c). These peptides appear to bind to specific receptors in and out of the cells, exerting various speculated biological effects.

The detectable concentration of Humanin in the skeletal muscles, hypothalamus, and cortex of murine models declined progressively with advancing age. Humanin may potentially be a subsequent biomarker of age. Humanin is suggested to have diverse biological functions, including cytoprotective and metabolic roles. Cytoprotective roles may involve protection against oxidative stress and injury, anti-inflammatory responses, neuroprotection, and cardioprotection. Metabolic protection roles may involve metabolic hemostasis, ATP production, reduction in visceral fat, and glucose-stimulated insulin secretion.

Myocardial fibrosis may appear either as an age-related physiological change or due to various pathological phenomena such as Myocardial Infarction and ischemic reperfusion injury, contributing to cardiac dysfunction. It is speculated to affect both systolic and diastolic function and eventually progress to heart failure. The number of fibroblast cells present in cardiac tissue may directly correlate with the age of the heart tissue. Considering its ratio to the cardiac striated cells present may indicate the extent of age-related degenerative change in the heart. These fibroblasts may lead to the secretion of extracellular matrix proteins such as collagen type 1 that favors fibrosis.

Humanin – Mechanism of Action

Studies suggest that Humanin may exert cardioprotective effects by activating the AKT/GSK-3 beta (Glycogen Synthase Kinase) pathway. Humanin might also be able to alter the pro-apoptotic factors in the cardiac fibers and prevent cell death, starting and downregulating varying pathways depending on the action site and the pathology type. Other factors considered to be responsible for causing fibrosis in the heart, such as FGF-2 (Fibroblast Growth Factor-2), MMP-2 (Matrix Metalloproteinase-2), and Transforming Growth Factor-beta (TGF-beta), may increase in the cardiac tissue as age progresses. Studies suggest the role of Humanin in attenuating the effect of them all.

Another speculated mechanism associated with age-related cardiac tissue deterioration involves the damage caused by Reactive Oxidative Species (ROS). Excessive Reactive Oxidative Species may cause the deterioration of the Antioxidant Defense System by depolarizing the mitochondrial membrane. This could lead to ATP (Adenosine Triphosphate) hydrolysis and the speculated swelling of the mitochondria. This might cause the rupture of the outer membrane of mitochondria and, eventually, the release of pro-apoptotic proteins in the cytosol. The Humanin peptide may induce enzymes and various small non-enzymatic molecules that lead to an overall reduction of the oxidative stress caused by Reactive Oxygen Species (ROS).

A study on aged rats propose that chronic exposure to exogenous Humanin may ameliorate myocardial fibrosis and apoptosis. This study indicate an increase in the ratio of cardiac fibers to fibroblasts, measured in the percentage of each cell present in a random field chosen after immunofluorescence staining of the cardiac tissue. Picrosirius red staining of the cardiac tissue might inducate a decrease in the collagen content of the heart tissue, a marker of tissue age. Long-term supplementation of Humanin may reduce fibroblast proliferation and downregulate the expression of Fibroblast Growth Factor-2 (FGF-2), Matrix Metalloproteinase-2 (MMP-2), and Transforming Growth Factor-beta 1 (TGF-beta 1). It has also been speculated to suppress pro-apoptotic factors in the cardiac tissue.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

ARA-290 is a peptide derivative from Erythropoietin (EPO). Erythropoietin, assumed to be the primary hormone responsible for erythropoiesis, may be involved in various physiological processes, including angiogenesis, cell survival, blood pressure regulation, and potential neuroprotection in diabetic neuropathy.

<a href=”https://biotechpeptides.com/product/ara-290-16mg/” title=”Buy ARA-290 – 16mg”><strong>ARA-290</strong></a> peptide is of interest to researchers due to its speculated selective range of effects on nociception and neuroprotection, while purportedly avoiding hemopoietic actions. Researchers may suggest that these properties may play a role in wound repair in diabetes and immune modulation in autoimmune diseases.

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<h2>Research Implications of ARA-290 Peptide:</h2>

<strong>1. Blood Vessel Integrity</strong> ARA-290 peptide may play a significant role, researchers suggest, in prolonging cell survival and aiding Endothelial Colony Forming Cells (ECFCs) to repair and rebuild blood vessels after their integrity may be compromised following an injury. Similarly, researchers propose that ARA-290 peptide might protect retinal epithelial cells from ischemic or inflammatory injury, potentially promoting repair and leading to regeneration. ARA-290 is speculated to improve the migration, proliferation, and homing ability of Endothelial Colony Forming Cells, favoring the targeted repair of damaged blood vessels. Studies suggest that the peptide augments the effect of endogenous ECFCs and the transplanted exogenous ECFCs to repair and establish the vasculature of ischemic tissues.

<strong>2. Downregulation of Inflammatory Cytokines and Tissue Protection</strong> Researchers suggest that ARA-290 has the potential to suppress the inflammatory cascade by inhibiting the release of TNF-alpha, IL-6, and IL-12, speculated to prolong the survival of exogenous islet cells in diabetes. The mechanism behind this inflammatory suppression may involve the binding of the ARA-290 peptide to the Tissue Protective Receptor (TPR), reducing the effect of harmful inflammatory mediators and potentially boosting tissue protection. While erythropoietin may play a similar role, ARA-290 peptide is speculated to offer better wound healing and quicker post-injury recovery without the hematopoietic and cardiovascular effects associated with erythropoietin.

<strong>3. Role of ARA-290 in Immune System Regulation</strong> There is mounting data to suggest a role of ARA-290 peptide in immune modulation, through the binding of ARA-290 to Tissue Protective Receptors, expressed by various immune cells. After binding, ARA-290 may be expected to suppress the release of proinflammatory mediators, reducing disease severity and preventing long-term morbidity due to chronic inflammation. It may also decrease the release of inflammatory chemokines by macrophages, potentially reducing inflammatory infiltration while favoring resident macrophage recruitment to the site of injury, preventing side effects of inflammation on surrounding tissues. Studies suggest the ARA-290 peptide may alter the antigenic property of dendritic cells, potentially leading to increased long-term resistance against pathogens. This may form the foundation of its role in preventing tissue, organ, or graft rejection following transplantation. Research suggest that ARA-290 peptide has an effect on reducing levels of ANA and anti-dsDNA in Systemic Lupus Erythematous (SLE), considered markers of disease progression.

<strong>4. Nociception</strong> Researchers suggest that neuropathic pain caused by diabetic neuropathy, which is difficult to control and poorly understood, might be alleviated by suppressing Innate Repair Receptors (IRR), on which ARA-290 peptide may act. This action may inhibit TRPV1 channel (Capsaicin receptor) activity, responsible for the perception of burning pain associated with neuropathy. Studies have suggested that ARA-290 peptide exposure may increase small nerve fiber density, significantly controlling pain associated with neuropathy in several autoimmune diseases, such as sarcoidosis, diabetes, and HIV.

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<em><strong>Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.</strong></em>

Kisspeptin-10 peptide is speculated to regulate several hormone-controlled activities. It is suggested to play a significant role in regulating the hypothalamo-pituitary-gonadal axis, which is deemed essential in pubarche. It may also play a role in the female reproductive cycle through negative feedback control of the gonadotropin-releasing hormone estrogen.

Potential Effects of Kisspeptin-10

1. Reduction in Fat Cell Storage Kisspeptin-10 has been suggested to potentially reduce the accumulation of fat cell storage by decreasing the formation and maturation of adipocytes. It might limit the formation of adipocytes by decreasing the expression of the PPAR-y and CEBP-beta genes involved in the construction and differentiation of adipocytes. Kisspeptin-10 has been speculated to affect the formation of fat cells and the breakdown of existing cells. It may enhance the expression of perilipin and hormone-sensitive lipase, the enzyme involved in the breakdown of fat cells. It may also reduce fat accumulation by potentially stimulating leptin, a hormone the adipocytes produce. Leptin may regulate energy balance by suppressing food intake through signals sent to the hypothalamus. When food intake is stopped, the fat reservoir may be utilized, and more fat cells may be broken down.
2. Bone Development Kisspeptin-10 (KP-10) may potentially help activate bone-forming cells known as osteoblasts. It may increase the genetic expression of osteogenesis such as the bone morphogenetic protein 2 (BMP2) genes. Kisspeptin-10 may also activate several transcription factors involved in osteoblasts’ activation. These transcription factors include Runt-related transcription factor 2 (Runx2), alkaline phosphatase (ALP), and distal–less homeobox 5 (Dlx5). The activated osteoblasts may then form bone cells (osteocytes). Once osteocytes undergo maturation and differentiation, they may lead to an increase in bone matrix formation and bone mineral density.
3. Control of Fertility Kisspeptin-10 may be important in regulating the hypothalamic-pituitary-gonadal (HPG) axis, which produces and regulates gonadal hormones like testosterone and estrogen. These hormones are considered to be responsible for the secondary sexual characteristics that accompany developmental maturation. Since 2005, Kisspeptin-10 has been speculated to be the most significant activator of the HPG axis. In a study, the exposure to Kisspeptin-10 appeared to have induced the rats’ maturation, while the exposure to its antagonist delayed their maturation.
4. Potential Neuronal Regeneration Gonadotropin-releasing hormone (GnRH) may exhibit neuroprotective and neuro-regenerative actions. The widespread incidence of GnRH and GnRH immune-reactive neurons in the cerebral cortex suggests that GnRH may be a neuromodulatory peptide. Immunohistochemistry studies also suggest the presence of a GnRH receptor and messenger RNA in the cerebral cortical neurons of rats’ embryos and adult rats. Kisspeptin-10 may stimulate and regulate the production of GnRH.
5. Kisspeptin-10 and Olfaction Olfaction may have a vital role to play in mammalian reproduction. Recent studies may have suggested that Kisspeptin-10 is present in the amygdala, the central structure of the olfactory system. Immunochemistry may also have revealed a close relationship between amygdala neurons containing Kisspeptin-10 and dopaminergic neurons, indicating the importance of Kisspeptin-10 in social behaviors like reward and motivation. A study may suggested that male mice exposed to Kisspeptin-10 spent most of their time sniffing female mice. In contrast, those given testosterone did not investigate females preferentially over males.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

Therefore, peptides may basically be described as smaller, simpler versions of proteins. Studies have suggested that they may affect immunomodulation, growth hormone release, extracellular matrix production, and nerve cell growth and migration. Peptides may be the key to starting and stopping important biochemical cascades and may therefore prove important for biological function.

Studies over the last few decades have suggested that peptides may act to regulate cell aging cycles, control inflammation, mitigate infection, facilitate progressive tissue repair, increase cognitive synapses, and alter body composition.

Peptide Research

Slowing Cell Aging

A handful of peptides, including Sermorelin and Epithalon, have been suggested to alter the cell aging cycle at the DNA level. These have been speculated to activate an enzyme called telomerase to protect and repair DNA endpoints (called telomeres). Telomere degradation over time is one of the major signals that cells use to determine whether they divide and grow.Cell division may stop if telomeres become too short, and tissues may deteriorate. Certain peptides have been researched for their potential to delay the rate of tissue destruction by protecting telomeres. They may also reduce oxidative damage. Such peptides include Sermorelin, Epithalon, Ipamorelin, CJC-1295, and BPC 157. These peptides are classified as antioxidants that may mitigate cancer cell proliferation, cardiac and cognitive dysfunction, and other conditions.
 

Rapid Tissue Repair

Peptides may improve wound healing by affecting the growth hormone axis, increasing cell migration rates, reducing inflammation, and deposition extracellular matrix components. Many peptides, such as VIP, KPV, BPC 157, Sermorelin, and Hexarelin, have been researched for their potential in this area. Studies have suggested that these peptides may exert antifibrotic action, and lend support to tissue repair processes. One such peptide, BPC157, is widely considered to exhibit tissue healing characteristics, especially in its potential to promote tendon regeneration. Tendons are considered to be slow menders, but studies have suggested that BPC157 may speed up the process. Other peptides, like TB-500 and KPV, have been suggested to exert antimicrobial action to help ensure sterile wound healing.
 

Lean Muscle Structure

Sermorelin, CJC 1295, GHRP2, etc., are all hypothesized to impact the growth hormone axis, inducing an increase in bone density and muscle mass while dissolving fat cell collections. Ipamorelin has been posited to exhibit similar characteristics but with improved bone strengthening.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

Tesamorelin is a peptide that researchers suggest holds importance in addressing cardiovascular disease in research models of HIV. Findings from studies propose that Tesamorelin peptide may be associated with a reduction in excess fat cell accumulation in models of HIV and lipodystrophy.

What is Tesamorelin Peptide?

Tesamorelin peptide, also known as (TH9507), is a synthetic growth hormone-releasing factor agonist that researchers suggest stimulates the production and release of endogenous growth hormone. Speculative information indicates that it consists of the 44 amino acids of Growth Hormone Releasing Hormone (GHRH) with the addition of a trans-3-hexenoic acid group. It is also speculated to be more potent and stable than GHRH and resistant to cleavage by the enzyme dipeptidyl aminopeptidase.

In animal experiments, it is suggested to have significantly reduced visceral adipose tissue (VAT). Researchers propose that Tesamorelin peptide was found to reduce triglycerides and total cholesterol in research models of lipodystrophy when introduced combinatorily with antiretroviral therapy in research models of HIV.

Structure of Tesamorelin Peptide

Sequence: Unk-Tyr-Ala-Asp-Ala-Ile-Phe-Thr-Asn-Ser-Tyr-Arg-Lys-Val-Leu-Gly-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Met-Ser-Arg-Gln-Gln-Gly-Glu-Ser-Asn-Gln-Glu-Arg-Gly-Ala-Arg-Ala-Arg-Leu-NH2

Molecular Formula: C₂₂₁H₃₆₆N₇₂O₆₇S

Molecular weight: 5136 g/molS

Tesamorelin Peptide Mechanism of Action

Research daata suggests that Tesamorelin peptide binds and stimulates GHRF receptors with similar efficacy to endogenous GHRF. Growth hormone-releasing factor is a hypothalamic peptide speculated to act on the somatotropic cells of the pituitary gland to stimulate the synthesis and pulsatile release of endogenous growth hormone. This growth hormone is speculated to be both anabolic and lipolytic, exerting effects on various target cells.

Studies propose that the main mechanism of action of Tesamorelin is lipolysis, the breakdown of lipids and triglycerides. Generally stored in the  for later energy use, high values for either may increase the risk of heart disease.

Case Study

A study involved Antiretroviral Therapy (ART) HIV research models with excess fat accumulation. These research models were given Tesamorelin  or placebo each day. After 26 weeks, the group of research subjects receiving placebo were switched to Tesamorelin peptide for the next 26 weeks. The exposure to Tesamorelin in the experimental group was continued for another 26 weeks. Observations from the study suggest that exposure to Tesamorelin may decrease Visceral Adipose Tissue (VAT) and maintain the reduction for up to 52 weeks, possibly maintaining abdominal adipose tissue, improving lipids and body image, and without any significant changes in glucose parameters.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

References

Falutz J, Mamputu JC, Potvin D, Moyle G, Soulban G, Loughrey H, Marsolais C, Turner R, Grinspoon S. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010 Sep;95(9):4291-304

PEG-MGF, or Pegylated Mechano Growth Factor, is a variant of IGF-1. PEG-ylation modifies MGF by fusing polyethylene glycol (PEG) into it, potentially extending its half-life from a few minutes to days, allowing it to travel through the bloodstream for an extended period before breaking down and being excreted by the kidneys. Researchers suggest this process is essential for animal muscle regeneration after physical exertion or injury by promoting nitrogen retention and increasing protein synthesis.

Mechanism of Action

Research data from animal studies suggests that PEG-MGF supports the regeneration process of muscle, positively regulates protein synthesis, and activates satellite cells. In experiments where the PEG-MGF cDNA has been inserted into a plasmid vector and introduced into muscle cells, it appears to be a potent inducer of muscle hypertrophy. The addition of PEG-MGF to muscle myoblasts appeared to have increased proliferation and delayed differentiation, even in the presence of anti – IGF 1 receptor antibodies, potentially by activating fibrinolysis of matrix and metalloproteinase systems. Additionally, researchers propose that intense physical exertion may stimulate the release of growth hormone in the muscles to release MGF, especially as levels of this hormone decrease over time. Furthermore, a recent study of PEG-MGF suggests that the activity of protein kinase C is speculated to be necessary for the activation of this peptide (translocation to the nucleus) of factor 2 related to NFE 2 (Nrf2). This, in turn, is suggested to increase the expression of heme oxygenase 1, an event speculated to mediate neuroprotection of neurons from oxidative stress-induced apoptosis in the brain.

Research into PEG-MGF

In addition to its potential effects on muscle, PEG-MGF is speculated to have other impacts in the bodies of animal research models. Researchers suggest that PEG-MGF may enhance the proliferation and migration of bone marrow-derived mesenchymal stem cells, which are suggested to be a source of autologous stem cells for transplantation to the heart. There is speculative evidence of transient regulation of PEG b MGF expression in response to myocardial infarction associated with ischemia in the heart. Intracoronary exposure to this peptide is suggested to induce myocardial protection and improve hemodynamic function more than mature IGF – 1 after myocardial infarction in sheep. The speculated cellular protection conferred by PEG-MGF is suggested to be based on the inhibition of apoptosis in the border area of the infarct. PEG-MGF has been suggested to stimulate proangiogenic activities in vascular endothelial cells. Therefore, it may confer potentially beneficial action at the level of vascular regeneration and collateralization to restore blood flow to the heart after myocardial infarction. IGF – 1, considered to play an essential role in the interface between neurons in injured or damaged muscles, has shown potential effectiveness in slowing the progression of amyotrophic lateral sclerosis (ALS), a disease characterized by the loss of motor neurons and progressive muscle weakness. Exposure to PEG-MGF has been reported to produce improvements, with more motor neurons surviving in PEG-MGF-treated mice. MGF may be expressed in excess in regenerating regions after global cerebral ischemia. Its transcripts, thought to be expressed during brain development, are suggested to exhibit particular time distributions. Additionally, neonatal hypoxia and insults of hypoxic ischemia are suggested to lead to increased and prolonged expression of only the MGF isoform.

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.