Add like
Add dislike
Add to saved papers

Liver Insulin-like Growth Factor-1 mediates effects of low-intensity vibration on wound healing in diabetic mice.

Journal of Pathology 2023 Februrary 21
Chronic wounds in diabetic patients are associated with significant morbidity and mortality; however, few therapies are available to improve healing of diabetic wounds. Our group previously reported that low-intensity vibration (LIV) can improve angiogenesis and wound healing in diabetic mice. The purpose of the current study was to begin to elucidate mechanisms underlying LIV-enhanced healing. We first demonstrate that LIV-enhanced wound healing in db/db mice is associated with increased IGF1 protein levels in liver, blood, and wounds. The increase in IGF1 protein in wounds is associated with increased Igf1 mRNA expression both in liver and wounds but the increase in protein levels preceded the increase in mRNA expression in wounds. Since our previous study demonstrated that liver is a primary source of IGF1 in skin wounds, we used inducible ablation of IGF1 in liver of high fat diet-fed (HFD) mice to determine whether liver IGF1 mediates the effects of LIV on wound healing. We demonstrate that knockdown of IGF1 in liver blunts LIV-induced improvements in wound healing in HFD mice, particularly increased angiogenesis and granulation tissue formation, and inhibits the resolution of inflammation. These studies indicate that LIV may promote skin wound healing at least in part via crosstalk between the liver and wound. This article is protected by copyright. All rights reserved.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app