Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes
Just came across this article concerning the proposed use of Annexin A1, an anti inflammation mediator, to prevent and treat inflammatory disease complications in T1 diabetes. It at least seems to work in diabetic mice. Could hold promise in reducing one of the scariest aspects of Diabetes.
This has potential if it makes it from mice to humans!
Furthermore, in mouse models with STZ-induced type 1 diabetes, ANXA1 protects against cardiac and renal dysfunction by returning MAPK signalling to baseline and activating pro-survival pathways (Akt).
These diabetic mice have all the luck 
After the researchers gave them diabetes 
There’s some observational info on humans in the study that I thought was interesting. "Plasma levels of ANXA1 were higher in individuals with diabetes with or without a diagnosis of diabetic nephropathy compared with healthy individuals (Fig. 1a)… Participants with diabetic nephropathy have higher plasma levels of CRP (a marker of systemic inflammation) compared with those with no nephropathy (Fig. 1b). "
Makes you wonder why the CRP differs if both groups have similar concentrations of ANXA1. Seems like they might be missing something… or maybe I missed something in the study.
I also couldn’t find any info on the A1cs of these humans.
Seems to me that T1’s in general have a higher concentration of of ANXA1 because of the inevitable at least slight increase in inflammatory processes.
CRP, the marker for inflammation they are following is only elevated when greater inflammation occurs from frank neuropathy. And a significant cohort of the T1D neuropathy group did have a higher level of ANXA1, likely in response to their increased inflammation.
I couldn’t find this for the humans. The charts above appear to show similar concentrations of ANXA1 for both T1DM groups. Could you direct me to a quote? I’m confused about how they came to the conclusion that ANXA1 might impact the development of nephropathy if both of these groups have similar concentrations of ANXA1 but the group with nephropathy has higher CRP levels.
I may have misspoken when I used the word “significant”, but in looking at the diagram it seems to me that there is at least a slight difference in endogenous ANXA1 in the neuropathy group.
But in the discussion section it pretty clearly lays out a compelling hypothesis that increased levels of the anti inflammation modulator ANAX1 would decrease the inflammatory marker CRP in humans.
I guess it needs a human study with larger groups.