A link to this article was posted over at stocktwits by Real_Highlander.
my response -
What caught my eye was that sPLA2-11A induces production of pro-inflammatory arachidonic acid which I've ran into repeatedly in my reading. CCL3, CCL4, CCL5, CCL7 and CCL8 (all blocked by leronlimab) also increase arachidonic acid by increase of CA2+. Arachidonic acid can induce reactive oxygen species (free radicals) which are implicated in Alzheimer's, hypertension, atherosclerosis, heart disease, diabetes and of interest to a recent trial, hepatic steatosis (NASH).
Reactive oxygen species also damage mitochondria as detailed in a previous post.
https://investorshangout.com/post/view?id=6231450
Quote:Does this enzyme raise the chance of COVID-related death?https://m.jpost.com/science/does-this-enzyme-...ath-678710
my response -
Quote:The enzyme they talk about sPLA2-11A may be a good biomarker for determining who will advance to severe or critical Covid. But they have it ass backwards by thinking that sPLA2-11A might raise the chance of death by Covid. Increased production of sPLA2-11A is caused by inflammatory cytokines IL-6, IL-1β and TNF-α. Leronlimab downregulates all three cytokines and so also sPLA2-11A, yet another way leronlimab lowers inflammation.
What caught my eye was that sPLA2-11A induces production of pro-inflammatory arachidonic acid which I've ran into repeatedly in my reading. CCL3, CCL4, CCL5, CCL7 and CCL8 (all blocked by leronlimab) also increase arachidonic acid by increase of CA2+. Arachidonic acid can induce reactive oxygen species (free radicals) which are implicated in Alzheimer's, hypertension, atherosclerosis, heart disease, diabetes and of interest to a recent trial, hepatic steatosis (NASH).
Quote:The involvement of eicosanoids in NAFLD and NASH has been established by several lines of evidence. First, genetic disruption of PLA2, the rate-limiting key enzyme in AA production, alleviates high-fat diet-induced hepatic steatosis and results in reduced PGE2 levels in mice.
Second, 5-LOX-derived LTs are implicated in the pathogenesis of NAFLD, as both mice and humans suffering from NAFLD demonstrate a significantly increased activity of the 5-LOX pathway, and the enhanced expression of 5-LOX derivatives correlates with the severity of the hepatic disease [173,174]. A disruption of the 5-LOX pathway in hyperlipidemic apolipoprotein E (apoE) deficient mice reduces hepatic inflammation and tumor necrosis factor alpha (TNFα) dependent hepatic injury
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274989/
Reactive oxygen species also damage mitochondria as detailed in a previous post.
https://investorshangout.com/post/view?id=6231450
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