The raging lung inflammation that can contribute to death from the flu can be stopped in its tracks by a drug derived from a naturally occurring human protein, a new animal study suggests.
In mouse studies, all untreated animals given a lethal dose of influenza died within days. All but one of the infected mice treated with the experimental therapy not only survived, but remained energetic and kept weight on – despite having high levels of the flu virus in their lungs.
The experimental treatment is a heavy dose of MG53, part of a family of proteins that plays an essential role in cell membrane repair. Already identified as a potential therapy for conditions ranging from Alzheimer’s disease to persistent skin wounds, MG53 was found in this study to prevent death from a lethal flu infection by blocking excessive inflammation – without having any effect on the virus itself.
When applied intravenously, rhMG53 ameliorates pathology associated with muscular dystrophy, lung injury, myocardial infarction, and acute kidney injury in rodent and large animal models of these diseases13,17,18,19. These data highlight the importance of targeting cell membrane repair in regenerative medicine and present MG53 as a potential biological reagent for restoration of tissue integrity in a broad range of human diseases.
A recent report by Liu et al. showed that cardiac-specific overexpression of MG53 induced cardiomyopathy via transcriptional activation of the peroxisome proliferation-activated receptor (PPARα)30. While these studies raise concerns over the safety of MG53 overexpression on cardiovascular and metabolic function, no studies have been conducted to investigate the physiological impact of elevating MG53 in blood circulation.
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