Maybe that analyst should start reading these articles... This article address the role of oxidative Stress (not being able to detoxify) and positive roll of oxidative phosphorylation (generating energy) on transition from NAFLD to NASH. Tesamorelin has positive impact on oxidative phosphorylation, inflammation, tissue repair, cell division and reduces oxidative stress.
In deed, lipid peroxidation, which is a common feature of NAFLD and NASH [11], generates oxidized phospholipids (provide barriers in cellular membranes to protect the cell), such as phosphocholine on oxidized phospholipids and oxidized cardiolipin, and reactive aldehydes, among which the most studied and best characterized are malondialdehyde (MDA) and 4hydroxynonenal (4HNE). Interestingly, both of these oxidative stressderived molecules act as direct inducers of hepatic inflammation [12] and as antigenic adducts (toxins) named oxidative stressderived epitopes or oxidationspecific epitopes (OSEs), by reacting with selfcellular macromolecules.
Targeting oxidized phospholipids has been suggested as a therapeutic strategy for the management of hepatic inflammation [18] and, more recently, for NASH [19]. Recently, it has also been demonstrated that OSEs can activate the innate immunity receptor for advanced glycation end products (RAGE) [20], a receptor interacting with ligands highly present during inflammation.
Taken together, these observations are consistent in picturing a fascinating scenario, in which oxidative stress and innate and adaptive immunity cooperate in generating and supporting hepatic inflammation, favoring the transition from NAFLD to NASH.
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