Mitochondrial dysfunction in Spaceflight Associated Neuro-Ocular Syndrome (SANS): a molecular hypothesis in pathogenesis
Ethan Waisberg, Joshua Ong, Mouayad Masalkhi, Xiao Wen Mao, Afshin Beheshti, Andrew G. Lee
Abstract
Spaceflight-associated neuro-ocular syndrome (SANS) is a condition affecting astronauts during long-duration spaceflight (LDSF). SANS is characterized by hyperopic refractive shifts [ 1 ], optic disc edema [ 2 ], globe flattening, and chorioretinal folds [ 3 ]. With the commercialization of human spaceflight, the amount of space travelers experiencing LDSF will grow exponentially over the coming years, and there may be a potential increase in cases of SANS. In addition, the planned crewed 2030 Mars Mission will expose astronauts to LDSF greater than previously experienced [ 4 ]. Although, the exact mechanisms underlying SANS is not fully understood, it is believed to be related to the unique environment of LDSF [ 5 ]. SANS has been traditionally linked to fluid shifts and structural changes in the eye caused by microgravity [ 5 ]. This hypothesis is based on that the absence of gravity in space leads to a redistribution of bodily fluids, resulting in increased intracranial pressure and subsequent changes in the eye [ 5 ]. However, recent research is exploring the role of mitochondrial dysfunction as a possible underlying cause of SANS [ 6 ].