Key result
Low-dose methylmercury worsens cardiac vulnerability to overload via filamin-dependent mitochondrial hyperfission.
Low-dose methylmercury exposure increases cardiac vulnerability to hemodynamic overload via mitochondrial hyperfission.
May warrant exposure caution in stressed hearts; hypothesis-generating for Drp1 pathways before human studies.
H by low-dose MeHg increases cardiac fragility to mechanical load through filamin-dependent mitochondrial hyperfission.
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Nishimura et al. (2019) studied this question. Depolysulfidation of Drp1 induced by low-dose methylmercury exposure increases cardiac vulnerability to hemodynamic overload via filamin-dependent mitochondrial hyperfission.
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