In vitro studies suggested that genistein treatment of human keratinocytes and fibroblasts modulates glutathione content and reactive oxygen species release, endothelial/inducible (e/i)NOS dependent nitric oxide release, MMP expression, and mitochondria membrane potential through mechanisms involving p38 MAPK, AKT and ERK1/2 as downstream signaling associated with membrane ERs and GPER, as well as by increasing SOD activity and BCL2 expression in endothelial cells (Savoia et al., 2018
8 min, 75% B
Massy, M., Marti, S., Hammer, H., & Hoepner, R
Type 2 DM Pathophysiology: T2DM involves the interplay of insulin resistance (primarily at skeletal muscle, liver, and adipose tissue) and progressive beta-cell secretory failure
Endothelial dysfunction in diabetes mellitus: molecular mechanisms and clinical implications
If one site becomes irritated, skip it entirely until it heals