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Its mechanism reflects modulation of the bodys built-in energy control architecture rather than forced metabolic acceleration

Overall, this group described a novel two-phase mechanism underlying hyperoxia-induced kidney damage in neonatal mice: an early acute injury phase modulated by renal growth inhibition via activation of IL-6/stat-3 and Smad2 (TGF-) signaling, and a late regenerative stage of accelerated growth leading to impaired glomerular and tubular function

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In addition, ROS-driven PF is positively correlated with cellular senescence, a process that may be exacerbated by the activation of the NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammasome (Figure 1)

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