In Situ Photo-Cross-Linking Hydrogel Accelerates Diabetic Wound Healing through Restored Hypoxia-Inducible Factor 1-Alpha Pathway and Regulated Inflammation

Stabilization of hypoxia-inducible factor-1 via novel minicircle vector improves diabetic wound healing

Journal of the American College of Surgeons ◽

10.1016/j.jamcollsurg.2011.06.411 ◽

2011 ◽

Vol 213 (3) ◽

pp. S88

Author(s):

Sae Hee Ko ◽

Shane Morrison ◽

Mei Huang ◽

Allison Nauta ◽

Geoffrey C. Gurtner ◽

...

Keyword(s):

Wound Healing ◽

Hypoxia Inducible Factor ◽

Diabetic Wound ◽

Hypoxia Inducible Factor 1 ◽

Diabetic Wound Healing

Download Full-text

Close-loop dynamic nanohybrids on collagen-ark with in situ gelling transformation capability for biomimetic stage-specific diabetic wound healing

Materials Horizons ◽

10.1039/c8mh01145a ◽

2019 ◽

Vol 6 (2) ◽

pp. 385-393 ◽

Cited By ~ 11

Author(s):

Zehua Liu ◽

Yunzhan Li ◽

Wei Li ◽

Wenhua Lian ◽

Marianna Kemell ◽

...

Keyword(s):

Wound Healing ◽

Porous Silicon ◽

Single Step ◽

Core Shell ◽

Diabetic Wound ◽

Nanoprecipitation Method ◽

Diabetic Wound Healing ◽

Core Shell Structure ◽

In Situ Gelling

A self-regulated dynamic nanohybrid that can sensitively respond to hyperglycemic microenvironment is developed. The nanohybrid with a core/shell structure is produced through a single-step microfluidics nanoprecipitation method, where drugs-loaded porous silicon (PSi) nanoparticles are encapsulated by H2O2 responsive polymeric matrix.

Download Full-text

Growth factor loaded in situ photocrosslinkable poly(3-hydroxybutyrate-co-3-hydroxyvalerate)/gelatin methacryloyl hybrid patch for diabetic wound healing

Materials Science and Engineering C ◽

10.1016/j.msec.2020.111519 ◽

2021 ◽

Vol 118 ◽

pp. 111519 ◽

Cited By ~ 3

Author(s):

Robin Augustine ◽

Anwarul Hasan ◽

Yogesh B. Dalvi ◽

Syed Raza Ur Rehman ◽

Ruby Varghese ◽

...

Keyword(s):

Wound Healing ◽

Growth Factor ◽

Diabetic Wound ◽

Diabetic Wound Healing

Download Full-text

In Situ Tissue Engineering Using Angiogenic Nanoscaffold Enhances Diabetic Wound Healing in db/db Mouse Model

ASME 2008 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2008-192198 ◽

2008 ◽

Author(s):

Swathi Balaji ◽

Sachin S. Vaikunth ◽

Jignesh K. Parvadia ◽

Timothy M. Crombleholme ◽

Daria A. Narmoneva

Keyword(s):

Tissue Engineering ◽

Wound Healing ◽

Attractive Alternative ◽

Diabetic Wound ◽

Diabetic Ulcer ◽

The Us ◽

Diabetic Wound Healing ◽

Bioengineered Skin ◽

Care Costs

Tissue engineering offers an attractive alternative for treatment of chronic nonhealing diabetic ulcers, which account for more than 27% of the $10.9 billion total diabetic health care costs in the US annually [1]. The harsh environment of a diabetic ulcer is characterized by reduced expression of angiogenic factors, insufficient vascularization, excess protease activity, matrix degradation and hyperglycemia-induced cell apoptosis [2]. A major factor contributing to insufficient neovascularization in diabetic nonhealing wounds may be deficiency in the recruitment of endothelial cells (ECs) and endothelial precursor cells (EPCs) to the wound site [3]. Recent studies focusing on altering the wound’s cellular and molecular environment using bone-marrow-derived stem cells, growth factors (delivered either directly or using gene or cell therapy), bioengineered skin constructs, and biological matrices, such as collagen and hyaluronic acid gels had promising wound healing outcomes [4]. These studies suggest that strategies aimed at modifying the extracellular environment of the diabetic wound to enhance cell survival and angiogenesis are promising for development of new therapies for diabetic wound healing.

Download Full-text

Liraglutide via Activation of AMP-Activated Protein Kinase-Hypoxia Inducible Factor-1α-Heme Oxygenase-1 Signaling Promotes Wound Healing by Preventing Endothelial Dysfunction in Diabetic Mice

Frontiers in Physiology ◽

10.3389/fphys.2021.660263 ◽

2021 ◽

Vol 12 ◽

Author(s):

Huiya Huang ◽

Linlin Wang ◽

Fanyu Qian ◽

Xiong Chen ◽

Haiping Zhu ◽

...

Keyword(s):

Wound Healing ◽

Protein Kinase ◽

Endothelial Dysfunction ◽

Heme Oxygenase ◽

Hypoxia Inducible Factor ◽

Heme Oxygenase 1 ◽

Diabetic Wound ◽

Hypoxia Inducible Factor 1Α ◽

Diabetic Wound Healing ◽

Amp Activated Protein Kinase

Background/Aims: Diabetic foot ulcers (DFUs) present a major challenge in clinical practice, and hyperglycemia-induced angiogenesis disturbance and endothelial dysfunction likely exacerbate DFUs. The long-acting glucagon-like peptide-1 (GLP-1) analog liraglutide (Lira) is a potential activator of AMP-activated protein kinase (AMPK) that appears to enhance endothelial function and have substantial pro-angiogenesis and antioxidant stress effects. Therefore, in this study, we aimed to investigate whether the protective role of Lira in diabetic wound healing acts against the mechanisms underlying hyperglycemia-induced endothelial dysfunction and angiogenesis disturbance.Methods: Accordingly, db/db mice were assessed after receiving subcutaneous Lira injections. We also cultured human umbilical vein endothelial cells (HUVECs) in either normal or high glucose (5.5 or 33 mM glucose, respectively) medium with or without Lira for 72 h.Results: An obvious inhibition of hyperglycemia-triggered endothelial dysfunction and angiogenesis disturbance was observed; follow by a promotion of diabetic wound healing under Lira treatment combined with restored hyperglycemia-impaired AMPK signaling pathway activity. AMPKα1/2 siRNA and Compound C (Cpd C), an inhibitor of AMPK, abolished both Lira-mediated endothelial protection and pro-angiogenesis action, as well as the diabetic wound healing promoted by Lira. Furthermore, hypoxia inducible factor-1α (Hif-1α; transcription factors of AMPK substrates) knockdown in HUVECs and db/db mice demonstrated that Lira activated AMPK to prevent hyperglycemia-triggered endothelial dysfunction and angiogenesis disturbance, with a subsequent promotion of diabetic wound healing that was Hif-1α–heme oxygenase-1 (HO-1) axis-dependent. Taken together, these findings reveal that the promotion of diabetic wound healing by Lira occurs via its AMPK-dependent endothelial protection and pro-angiogenic effects, which are regulated by the Hif-1α–HO-1 axis.

Download Full-text