Mechanism Of Action

Mechanism Of Action

It's been discovered that erythropoietin works by binding to the erythropoietin receptor (EpoR). EPO (Epo antibody) triggers a JAK2 signaling cascade by binding to the erythropoietin receptor on the surface of red cell progenitors. The STAT5, PIK3, and Ras MAPK pathways are all activated as a result of this. The erythroid cell differentiates, survives, and proliferates as a result of this. Negative regulators of the cytokine signal, SOCS1, SOCS3, and CIS, are also expressed.

Erythropoietin receptor expression is highly concentrated in erythroid progenitor cells. While there have been reports of EPO receptors being detected in a variety of other tissues, including the heart, muscle, kidney, and peripheral/central nerve tissue, these findings have been muddled by the nonspecificity of reagents like anti-EpoR antibodies. A functioning EPO receptor was not found in those tissues in controlled trials. Because red blood cells lack the erythropoietin receptor, they cannot respond to EPO in the bloodstream.

History

Paul Carnot suggested the hypothesis that a hormone controls red blood cell synthesis in 1905. Carnot and his doctoral student Clotilde-Camille Deflandre attributed an increase in red blood cells in rabbit animals to a hemotropic substance termed hemopoietin after conducting studies on rabbits subjected to bloodletting. The hemopoietic substance was given the name erythropoietin by Eva Bonsdorff and Eeva Jalavisto. Allan J. Erslev and K.R. Reissman demonstrated that a chemical circulated in the blood can stimulate red blood cell synthesis and increase hematocrit. Erythropoietin was refined and confirmed as the substance.