Preprint Article Version 1 This version is not peer-reviewed

Omega-3 polyunsaturated fatty acids protect against ischemia-reperfusion renal injury through AMPK-mediated autophagy

Version 1 : Received: 3 August 2017 / Approved: 4 August 2017 / Online: 4 August 2017 (12:56:08 CEST)

A peer-reviewed article of this Preprint also exists.

Gwon, D.H.; Hwang, T.W.; Ro, J.-Y.; Kang, Y.-J.; Jeong, J.Y.; Kim, D.-K.; Lim, K.; Kim, D.W.; Choi, D.E.; Kim, J.-J. High Endogenous Accumulation of ω-3 Polyunsaturated Fatty Acids Protect against Ischemia-Reperfusion Renal Injury through AMPK-Mediated Autophagy in Fat-1 Mice. Int. J. Mol. Sci. 2017, 18, 2081. Gwon, D.H.; Hwang, T.W.; Ro, J.-Y.; Kang, Y.-J.; Jeong, J.Y.; Kim, D.-K.; Lim, K.; Kim, D.W.; Choi, D.E.; Kim, J.-J. High Endogenous Accumulation of ω-3 Polyunsaturated Fatty Acids Protect against Ischemia-Reperfusion Renal Injury through AMPK-Mediated Autophagy in Fat-1 Mice. Int. J. Mol. Sci. 2017, 18, 2081.

Journal reference: Int. J. Mol. Sci. 2017, 18, 2081
DOI: 10.3390/ijms18102081

Abstract

Regulated autophagy is involved in the repair of renal ischemia-reperfusion injury (IRI). ω3-Polyunsaturated fatty acids (ω3-PUFAs) show protective effects against various renal injuries. It was recently reported that ω3-PUFAs regulate autophagy. We assessed whether ω3-PUFAs attenuated IR-induced acute kidney injury (AKI) and evaluated associated mechanisms. C57Bl/6 background fat-1 mice and wild-type mice (wt) were divided into four groups: wt sham (n = 10), fat-1 sham (n = 10), wt IRI (reperfusion 35 min after clamping both the renal artery and vein; n = 15), and fat-1 IRI (n = 15). Kidneys and blood were harvested 24 h after IRI. Renal histological and molecular data were collected. The kidneys of fat-1 mice showed better renal cell survival, renal function, and pathological damage than those of wt mice after IRI. In addition, fat-1 mice showed less oxidative stress and autophagy impairment; greater amounts of LC3, Beclin-1, and Atg7; lower amounts of p62; and higher levels of renal cathepsin D and ATP6E than wt kidneys. They also showed more AMPK activation, which resulted in the inhibition of phosphorylation of the mammalian target of rapamycin (mTOR). Collectively, ω3-PUFAs in fat-1 mice contributed to AMPK mediated autophagy activation, leading to a renoprotective response.

Subject Areas

ischemia-reperfusion injury (IRI), ω3-PUFA, AMP-activated protein kinase (AMPK), autophagy

Readers' Comments and Ratings (0)

Leave a public comment
Send a private comment to the author(s)
Rate this article
Views 0
Downloads 0
Comments 0
Metrics 0
Leave a public comment

×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.