Endometriosis Cell Counts and Lesions Reduced by Vitamin A-like Compound in Early Study

Endometriosis Cell Counts and Lesions Reduced by Vitamin A-like Compound in Early Study

Research investigating fenretinide, a synthetic retinoid analogue, found it effective in inducing the death of endometriotic cells and in reducing the volume of endometriotic lesions. These results indicate that targeting the retinoid acid signaling pathway may be a promising strategy to treat endometriotic lesions. The study, titled “Fenretinide: a potential treatment for endometriosis,” was published in Fertility and Sterility.

Several studies have reported that the biosynthesis and metabolism of retinoids, compounds derived from vitamin A (retinol) that play key roles in cell growth and apoptosis (cell death), are impaired in endometriosis. Decreased retinoid production in endometriotic tissues has been associated with deficient estrogen metabolism and resistance to apoptosis by endometriotic cells. Moreover, previous studies have pointed to the potential benefit of retinoic acid in the treatment and suppression of endometrial lesions.

Researchers assessed the efficacy of fenretinide to induce apoptosis of human endometriotic cells in vitro and to decrease the volume of endometriotic lesions in vivo. Fenretinide, a synthetic retinoid analogue with decreased toxicity when compared to other similar compounds, has been shown to induce apoptosis in several cell and tissue types.

By assessing apoptosis and the expression of genes involved in retinoic acid signaling both in vitro and in mice implanted with endometriotic tissue, researchers observed that fenretinide treatment significantly increased apoptosis, decreasing cell count and viability. Moreover, it increased expression of a gene involved in retinoid uptake (STRA6), while the expression of genes involved in retinoid action (CRABP2 and FABP5) remained unchanged. Fenretinide treatment was also seen to significantly decrease endometriotic lesion volume in mice treated with the retinoid analogue for two weeks.

“Fenretinide appears to increase retinol uptake in endometriotic stromal cells by increasing STRA6 expression, and potentially reversing the pathological loss of retinoid availability. Treatment with this compound induces apoptosis. Targeting the retinoic acid signaling pathway may be a promising novel treatment for women suffering with endometriosis,” the authors concluded in their study.

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