The capability of the liver to fully regenerate after injury is a unique phenomenon essential for the maintenance of its important functions in the control of metabolism and xenobiotic detoxification.

Liver regeneration is the process by which the liver is able to replace lost liver tissue from growth from the remaining tissue. The liver is the only visceral organ that possesses the capacity to regenerate.[1][2] The liver can regenerate after either surgical removal or after chemical injury.[3] It is known that as little as 25% of the original liver mass can regenerate back to its full size.[2][4] The process of regeneration in mammals is mainly compensatory growth because only the mass of the liver is replaced, not the shape.[5]

Interleukin 6, IGF1, TNFa, VEGF, HGF, EGF, Klotho, Tropoelastin, eNOS Sonic Hedgehog, CXCL5, Neurogenin 3, Follistatin, FGF, WnT proteins, TGFb, Jagged, Delta and Notch proteins, Activins, BMPs, SDF1, PDGF, HIF1a.

TNFα and IL-6 are thought to play major roles in initiating the process of liver regeneration.

Liver regeneration is a highly organized tissue regrowth process and is the most important reaction of the liver to injury. The overall process of liver regeneration includes three phases: priming stage, proliferative phase, and termination phase. The initial step aims to induce hepatocytes to be sensitive to growth factors with the aid of some cytokines, including TNF-α and IL-6. The proliferation phase promotes hepatocytes to re-enter G1 with the stimulation of growth factors. While during the termination stage, hepatocytes will discontinue to proliferate to maintain normal liver mass and function. Except for cytokine- and growth factor-mediated pathways involved in regulating liver regeneration, new substances and technologies may emerge through further research to influence the regenerative process.

Using a direct conductive lead or nerve pathways a bioelectric stimulator delivers to the liver a series of bioelectric signaling sequences that home reparative stem cells to the liver, grow new blood supply, release regenerative proteins and differentiated stem cells into living functioning new liver tissue.

In addition to bioelectric stimulation therapy a re-fillable micro infusion pump is used (often with two chambers) to deliver slow infusions directly or nearly directly into the liver of the LC-15 fifteen component liver regeneration composition comprised of adipose tissue derived cells and stromal fraction, PRF, regenerative fluid derived from amniotic sourcing, micro RNA gel, selected growth factors, growth hormone, selected exosomes, oxygenated nanoparticles, nutrient hydrogel, selected alkaloids and liver matrix. The biologics therapy may be supplemented with patient specific liver cells harvested, cultured and multiple in a laboratory and re-injected into the patient via a re-fillable slow infusion micro pump.

Non-Invasive delivery of bioelectric signaling sequences and in severe cases IV infusion of the LC-15 cocktail composition for liver regeneration.

Home/recruit stem cells from a patient’s own bone marrow, fat tissue and circulating blood to their liver.

Klotho is a known anti-aging protein with powerful regeneration support capabilities is required for FGF19 binding to FGFR4, intracellular signaling, and downstream modulation of gene expression in regenerating livers.

Hedgehog signaling is critical for normal liver regeneration.

IGF-I is expressed in virtually every tissue of the body, but with much higher expression in the liver than in any other tissue. GH is a member of the cytokine superfamily of polypeptide regulators (13). The growth-promoting effects of GH can be direct in selected target tissues, such as liver, or indirectly, via its endocrine mediator IGF-I. GH is the primary regulator of IGF-I synthesis and secretion in hepatocytes; in turn, IGF-I regulates GH secretion IGF1 and GH play a major role in the process of liver regeneration. Recent studies have clarified the essential roles of GH and IGF-I in the liver. GH profoundly reduces visceral fat, which plays an important role in the development of NAFLD. Furthermore, GH directly reduces lipogenesis in the hepatocytes. IGF-I induces cellular senescence and inactivates hepatic stellate cells, therefore ameliorating fibrosis. IGF-I treatment has been shown to improve animal models of NASH and cirrhosis, suggesting potential clinical applications of IGF-I in these conditions.