Recently, we considered whether the MMT process plays a role in other peritoneal pathologies such as peritoneal metastasis and postsurgical adhesions. Peritoneal metastasis is a complication of abdominal carcinomas (e.g. ovarian carcinoma) for which there is no effective therapy. Progression of the metastatic implants is affected by CAFs, which can derive from different cell types. We have shown in human peritoneal implant biopsies that a subpopulation of CAFs derives from mesothelial cells through MMT. Our results also suggest that MMT renders the peritoneum more receptive to implantation of tumor cells, contributes to the growth and vascularization of secondary tumors and that MMT is a therapeutic target in peritoneal carcinomatosis.

Adhesions are areas of fibrotic tissue that bind tissues and organs that would normally not be connected, and can be seriously life-threatening. Most adhesions are postsurgical. Histological analyses of human postsurgical adhesions have demonstrated that the mesothelial cells adjacent to the fibrotic tissue show signs of an MMT, suggesting that this could be an initial step in their development. The physiopathological processes involved in their formation remain unknown. Recent results have shown that mechanical injury is the main inducer of MMT during the formation of adhesions. Consequently, molecules involved in mechano-transduction, such as caveolin 1 (CAV-1), could play a role in the modulation of mechanical MMT and adhesion formation.

The aim of our work is to expand the knowledge of the pathological implications of the MMT of mesothelial cells and the molecular mechanisms that regulate this process, and to identify molecular targets for the design of therapeutic strategies, with possible applications in diseases associated with peritoneal fibrosis/angiogenesis, and in peritoneal metastasis.