Platelet-activating factor acetylhydrolase and premature ovarian failure

Premature ovarian failure (POF) appears to be a complex disease entity with several underlying etiopathogenic contributions including the possibility of multiple distinctly different autoimmune mechanisms, in which inflammatory autoimmunity targeted to ovarian-specific germline antigens (e.g., zona pellucida proteins or Mater) or differentiation/regulatory factors (e.g. inhibin-alpha) were regarded as one of the most crucial factors. Platelet-activating factor (PAF) and PAF class oxidized phospholipids stimulate the occurrence and development of inflammation and atherosclerosis. PAF acetylhydrolase (PAF-AH) can hydrolyze PAF and PAF class oxidized phospholipids and eventually prevent the body from the damage of these inflammatory mediators. These findings indicate a potential relationship between PAF-AH and POF thus have major implications for the future health of women who suffer with premature ovarian failure.