As commented in a recent review [94], the investigation of Beclin-1-mediated cardiac protection during endotoxemia suggests that enhancing Beclin-1 signal in cardiomyocytes mitigates inflammation by suppressing the release of mitochondrial DAMPs via PINK1/Parkin mitophagy, which may in turn interrupt local inflammatory circuitries, reduce neutrophil infiltration, and inhibit further cytokine production by leukocytes and non-myocytes such as fibroblasts. Here, PRKN is linked to serum lipopolysaccharide activity.