DcR3 is the Main Cause of Endometriosis

Dr. Shi-Liang Hsieh’s team has done years of searching in order to find answers to inflammations. Lately his team has unveiled a new role of the DcR3 protein molecule and published their finding in the Journal of Pathology.

Menstrual cramps is not an unfamiliar matter for half of the world population. Most women, if not have experienced it, would have known it from her female friends. Although there may be various reasons of a cramp, if the pain is caused Endometriosis, one should probably not just take a pain killer and wish it’ll go away someday.

Endometriosis is a symptom when tissue cells of the uterus travel into the pelvic area and flourish outside the ovary. Besides pelvic pain, it may lead to infertility.

DcR3 has been a target for Cancer studies, there were reports illustrating its role in enhancing cancer cell growths. Curiosity has led Hsieh’s team to explore its role in other areas. So far they have already identified the goodness of CdR3 in cases of regenerating damaged spinal cells, in Alzheimer’s disease when DcR3 proved to reduce Amyloid-β. The latest finding adds more mystery to DcR3, however, as the mechanism of Endometriosis is finally revealed, a root-cause solution is promising.

The study was carried out in collaboration with Dr. Yi-Jen Chen of Taipei Veterans General Hospital and Dr. Hsiao-Wen Tsai of Kaohsiung Veterans General Hospital.



First, by comparing clinical data, DcR3 was definitely over expressed in Endometriosis patients. It was even more startling when later they saw how wildly the Endometrium tumor would grow in transgenic mice. From their experiment, it appeared that DcR3 has a way to promotes cell adhesion and thus providing endometriosis development a solid ground. On the other hand, knocking down of DcR3 down regulates the expression of ICAM-1 and HCAM, which are the cells that make endometrium cells adhesive, thus reduces cell adhesion and migration.

The study suggests DcR3 plays a critical role in the pathogenesis of endometriosis, and inhibition of DcR3 expression is a promising approach for the treatment of endometriosis.

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