Experimental data showed promising results regarding the application of low-dose carbon monoxide in preclinical models of ARDS [16, 59, 78,79,80,81,82], including some mechanistic considerations, such as the induction of autophagy, the inhibition of mitochondrial dysfunction, inflammasome activation, and an accelerated resolution of the inflammation via special pro-resolving mediators [80, 83,84,85]
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