Pathophysiology of Renal erythropoietin- cells
This special issue belongs to |
Research & Reviews : Journal of Medical Science and Technology |
Related section |
NA |
Deadline for Manuscript Submission |
March 31st, 2023 |
Deadline for Publication |
April 15, 2023 |
Special Issue Description
Dear Collegues,
Chronic kidney illness (CKD) is an issue all over the world with expanding rate and prevalence. Iron deficiency, a well-known complication in CKD, is more visits in patients with lower glomerular filtration rates, particularly those with end-stage renal disease (ESRD) requiring long-term dialysis. Given that renal iron deficiency unfavorably influences the quality of life and is related to destitute results in CKD. Erythropoietin (EPO), a glycoprotein hormone, is the ace controller of erythropoiesis.
Later progresses in understanding the physiology and pathophysiology of renal EPO-producing cells (REPCs) give openings to find novel medications by upgrading oxygen detecting instruments and epigenetic modification. Anemia may be a common complication and contributes to expanded horribleness and mortality in constant kidney infection (CKD) patients. Though there has been a noteworthy enhancement in of understanding the fundamental component of erythropoiesis, the treatment of renal frailty is still confined to erythropoietin (EPO)-stimulating operators. The physiology of erythropoiesis, a useful part of EPO, and the fundamental atomic and cellular premise that directs EPO generation. In CKD, plasma EPO level is out of the extent to the degree of anemia.
In CKD, pericytes transdifferentiate to myofibroblasts, and hence the capacity of EPO generation diminishes, driving renal iron deficiency. Later exploratory and clinical considerations appear to the promising viability of prolyl hydroxylase inhibitors in renal iron deficiency through expanding EPO generation by stabilizing hypoxia-inducible factor (HIF).
Keywords
*Chronic kidney illness (CKD) *End-stage renal disease (ESRD) *Erythropoietin (EPO) *Renal EPO-producing cells (REPCs) *Epigenetic *Anemia *hypoxia-inducible factor (HIF)
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