![]() ![]() ![]() The innate immune response can be activated by LPS through the activation of TLR4 receptors, leading to the transcription of MyD88-dependent genes, which encode proinflammatory cytokines including inactive proforms of IL-1 β and inflammasome components. ![]() Multiple studies elucidated the role of the Fas/FasL system in the extrinsic epithelial apoptosis in LPS-induced ALI. DNA damage, hypoxia, and metabolic stress can induce intrinsic apoptosis, which begins with mitochondrial outer membrane permeabilization (MOMP) and leads to the release of mitochondrial proteins into the cytosol. The ROS may stimulate the cell death pathways and trigger inflammation, resulting in inflammasome activation, pyroptosis, and intrinsic apoptosis. Ischemia-reperfusion injury (IRI) refers to the irreversible tissue damage caused by insufficient oxygen supply following tissue ischemia and subsequent restoration of blood supply. Oxidative stress, inflammation, and calcium ion overload were involved with the ischemia-reperfusion injury. Ischemic preconditioning (IPC) is currently known as an effective protection strategy against the IRI. ![]()
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