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Mice Skin Wound - Europe PMC

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Last Updated: 09 May 2022

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STING activation promotes inflammatory response and delays skin wound healing in diabetic mice.

Sussive inflammatory responses delay wound healing in diabetic skin. STING activation has been identified as a pathogenic marker that is linked to delayed wound repair in diabetic skin, as shown by this article. Firstly, we discovered that STING expression has been enhanced in the epidermis of STZ-induced diabetes mouse model and db/db mouse model. With the high-glucose treatment, we also found that STING expression was upregulated in keratinocytes. In addition, silencing STING promoted wound healing in vitro. In addition, we found that autophagy dysfunction is linked to the development of STING in diabetic mice's epidermis.

Source link: https://europepmc.org/article/MED/35487062


Elevated skin senescence in young mice causes delayed wound healing.

Although increasing evidence that cellular senescence contributes to wound healing, wound healing is uncertain, a good and/or detrimental understanding of how senescence can be helpful and/or detrimental to wound healing is uncertain. Wound healing can also be influenced by baseline tissue senescence, which is elevated in aging and chronic wounds, both of which have significant healing times. We developed an elevated skin senescence model based on the subcutaneous transfer of irradiated fibroblasts into young 8-week-old wild-type C57BL/6 male mice to investigate wound healing. Skin senescence increased significantly during skin senescence rates compared to control transfers of non-irradiated fibroblasts. After healing, we discovered that states of elevated skin senescence could senescence delay wound healing and result in sustained senescence. Hence, the accumulation of senescent cells in aged skin or chronic wounds may be a source of delayed healing, and can be viewed as a potential target to improve healing.

Source link: https://europepmc.org/article/MED/35399134


Molecular mechanisms of skin wound healing in non-diabetic and diabetic mice in excision and pressure experimental wounds.

Experimental models for chronic skin lesions include excision and pressure ulcer, which are both "open" and "closed" lesions, respectively, but only the latter are defined by tissue hypoxia. An increase in VEGF receptor Kdr expression was discovered as well as the PI3K-Akt signaling pathway at the heart of the modified molecular network, as shown by the corresponding molecular network. Overall, the molecular review indicates that db/db mice have a longer inflammatory phase of the wound repair process, delaying the transition toward the proliferation and remodeling phases.

Source link: https://europepmc.org/article/MED/35386010


Improvement of Skin Wound Healing for Diabetic Mice with Thermosensitive Hydrogel Combined with Insulin Injection.

Diabetes-related skin inflammation is extremely common around the world. At 7, 14, 28, and 28 days, real-time quantitative polymerase chain reactions were performed to determine the relative expression of smooth muscle actin and transforming growth factor beta 1 in wound tissue. Compared to DControl and Poxin animals, wound closure and healing rate were dramatic during the first 7 days postoperative, but a significant decline on day 14 revealed an accelerated wound closure and healing rate. We therefore discovered that hydrogel and insulin stimulate wound healing. Antenneding of the expression of -SMA and TGF-1 in the early phase makes controlling the glucose level via insulin injection more effective than hydrogel alone for healing chronic wounds.

Source link: https://europepmc.org/article/MED/35311032

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions