FIGURE 1.

The potential effects of endometriosis on granulosa cells. Endometriosis might affect steroidogenesis (aromatase, StAR, 3β‐HSD), cytokine production (IL6, IL‐8, IL‐12, TNF‐ α), cell cycle progression, ER‐α/ PR, oxidative stress, ER stress, apoptosis, senescence, and autophagy in granulosa cells. The granulosa cells in women with endometriosis showed increased oxidative stress, which induced DNA damage, and decreased the mitochondrial membrane potential and ATP production and induced apoptosis. The increased TNF‐α activated NF‐κβ to decrease the telomerase activity and hTERT. TNF‐α also induced extrinsic and intrinsic apoptosis pathway and decreased survivin expression. The increased oxidative stress in the granulosa cells in women with endometriosis stimulated senescence and apoptosis through ER stress. StAR, steroidogenic acute regulatory protein; 3β‐HSD, 3β‐hydroxysteroid dehydrogenase; IL‐6, interleukin‐6; IL‐8, interleukin‐8; IL‐12, interleukin‐12; TNF‐α, tumor necrosis factor α; ER‐α, estrogen receptor‐ α ; PR, progesterone receptor; NF‐κB, nuclear factor‐κB.; hTERT, human telomerase reverse transcriptase, ER stress, endoplasmic reticulum stress; BECN1, beclin‐1. This figure was created with BioRender.com