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| http://dx.doi.org/10.1016/j.jid.2023.11.005 | DOI Listing |
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AP39, a novel mitochondria-targeted hydrogen sulfide donor, promotes cutaneous wound healing in an in vivo murine model of acute frostbite injury.
Biomed Pharmacother
January 2025
Department of Surgery, Division of Urology, London Health Sciences Center, Western University, London, Ontario, Canada; Matthew Mailing Center for Translational Transplant Studies, London Health Sciences Center, Western University, London, Ontario, Canada; Multi-Organ Transplant Program, London Health Sciences Center, Western University, London, Ontario, Canada; Department of Microbiology & Immunology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada. Electronic address:
Frostbite injury refers to cold tissue injury which typically affects the peripheral areas of the body, and is associated with limb loss and high rates of morbidity. Historically, treatment options have been limited to supportive care, leading to suboptimal outcomes for affected patients. The pathophysiology of frostbite injury has been understood in recent years to share similarity with that of cold ischemia-reperfusion injury as seen in solid organ transplantation, of which mitochondria play an important contributing role.
View Article and Find Full Text PDFBlockade of neddylation through targeted inhibition of DCN1 alleviates renal fibrosis.
Clin Sci (Lond)
January 2025
Zhengzhou University First Affiliated Hospital, Zhengzhou, China.
Neddylation is a process of attaching neuronal precursor cell-expressed developmentally downregulated protein 8 (NEDD8) to substrates for the protein function modulation via enzymatic cascades involving NEDD8-activating enzyme (E1), NEDD8-conjugating enzyme (E2), and NEDD8 ligase (E3). Defective in cullin neddylation 1 (DCN1) serves as a co-E3 ligase, that can simultaneously bind E2 UBE2M and cullin proteins to stabilize the catalytic center of the Cullin-Ring E3 ligase (CRL) complex, thereby promoting cullin neddylation. Neddylation is reported to be activated in diverse human diseases, and inhibition of protein neddylation has been regarded as a promising anticancer therapy.
View Article and Find Full Text PDFTalin, a Rap1 effector for integrin activation at the plasma membrane, also promotes Rap1 activity by disrupting sequestration of Rap1 by SHANK3.
J Cell Sci
January 2025
Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Talin regulates the adhesion and migration of cells in part by promoting the affinity of integrins for extracellular matrix proteins, a process that in cells such as endothelial cells and platelets requires the direct interaction of talin with both the small GTPase, Rap1-GTP, and the integrin β3 cytoplasmic tail. To study this process in more detail, we employed an optogenetic approach in living, immortalized endothelial cells to be able to regulate talin interaction with the plasma membrane. Previous studies identified talin as the Rap1-GTP effector for β3 integrin activation.
View Article and Find Full Text PDFPerch Hydrolysates from Upcycling of Perch Side Streams Accelerate Wound Healing by Enhancing Fibroblasts to Secrete Procollagen I, Fibronectin, and Hyaluronan.
Curr Issues Mol Biol
January 2025
Department of Nursing, Yuanpei University of Medical Technology, Hsinchu 300, Taiwan.
Wound healing incurs various challenges, making it an important topic in medicine. Short-chain peptides from fish protein hydrolysates possess wound healing properties that may represent a solution. In this study, perch hydrolysates were produced from perch side steams using a designed commercial complex enzyme via a proprietary pressure extraction technique.
View Article and Find Full Text PDFMechanically regulated microcarriers with stem cell loading for skin photoaging therapy.
Bioact Mater
April 2025
Department of Gastrointestinal Surgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou, 325035, China.
Long-term exposure to ultraviolet radiation compromises skin structural integrity and results in disruption of normal physiological functions. Stem cells have gained attention in anti-photoaging, while controlling the tissue mechanical microenvironment of cell delivery sites is crucial for regulating cell fate and achieving optimal therapeutic performances. Here, we introduce a mechanically regulated human recombinant collagen (RHC) microcarrier generated through microfluidics, which is capable of modulating stem cell differentiation to treat photoaged skin.
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