Song Gong

Background: Keloid formation is a multifaceted biological response to skin injury characterized by fibrous connective tissue, and functional and aesthetic impairments. Recent research highlights the role of plasma lipidomes in various diseases, yet their specific relationship with keloid formation has not been extensively studied. Objective: This study aims to elucidate the causal relationship between plasma lipidomes and keloid formation using a two-sample Mendelian randomization (MR) approach. Methods: Firstly, we employed a two-sample MR framework, utilizing genetic instrumental variables (IVs) derived from large-scale genome-wide association studies (GWAS). The exposure data comprised 179 plasma lipid species measured in 7174 individuals of European ancestry, while outcome data on keloids were sourced from a GWAS involving 436,200 individuals. IVs were selected using a significance threshold of P < 1× 10^{− 5} and linkage disequilibrium criteria, yielding 4507 independent single-nucleotide polymorphisms (SNPs). Causal effect estimates were calculated using multiple MR methods, and sensitivity analyses were conducted to evaluate the robustness of the findings. Results: The analysis suggested a significant association between elevated levels of Phosphatidylcholine (O-16:0_16:0) and increased risk of keloid formation (OR 1.399, 95% CI 1.166– 1.678, p-value < 0.001) by Inverse-variance weighted (IVW). Sensitivity analyses confirmed the absence of heterogeneity and significant horizontal pleiotropy, reinforcing the validity of the causal inference. Conclusion: Our findings indicate that specific lipid species, particularly Phosphatidylcholine, may be associated with an increased risk of keloid formation, highlighting a potential role of lipid metabolism in keloid pathophysiology.

Aim: Glucagon‐like peptide‐1 receptor agonists (GLP‐1RAs) hold clinical promise in promoting wound healing. This study investigated the pro‐healing effect and potential molecular mechanism of polyethylene glycol loxenatide (PEG‐Lox). Materials and Methods: HaCaT cells were incubated in high glucose (HG) condition with or without PEG‐Lox. Cell proliferation and viability were assessed by Cell Counting Kit 8 (CCK8) assay and PI staining. Cell migration was evaluated via Transwell and scratch wound healing assays. Transcriptomic analysis was conducted to identify the potential differentially expressed genes (DEGs). Western blotting was performed to validate protein expression levels of identified DEGs. Results: Cell proliferation and viability were significantly improved in the PEG‐Lox‐treated group when compared with the control group. Transwell assay showed that HG inhibited the migration of HaCaT cells, whereas PEG‐Lox treatment markedly resulted in a 1.7‐fold increase in the number of migrating cells ( p < 0.0001). The scratch closure rate was 32.83% after PEG‐Lox intervention, which was higher than that in the control group (24.42%, p < 0.001). Transcriptomic analysis found early growth response factor 1 (EGR1) to be the key DEG under PEG‐Lox treatment. The inhibition of PI3K/AKT signaling pathway by LY294002 down‐regulated the expression of EGR1 and impaired the proliferation and migration of HaCaT cells. Conclusions: Our study suggested that GLP‐1RA PEG‐Lox could promote wound healing by activating the PI3K/AKT/EGR1 signaling pathway, which further uncovered the potential pro‐healing effect of GLP‐1RAs in wounds.

Low-oxygen (O₂) environments are essential in various research and application fields, yet traditional methods like nitrogen flushing or chemical O₂ absorbers face challenges in high equipment cost and low controllability. This study introduces a novel electrochemical oxygen removal (EOR) controller, offering a lightweight, low-cost, and precise low-O₂ control solution. The self-powered EOR controller uses a sacrificial anode to drive the cathodic oxygen reduction reaction (ORR), efficiently consuming environmental O₂ to reduce its level, thus eliminating the requirements of external gas or power sources. By integrating a single-atom ORR catalyst and flexible design, the device achieves a substantial reduction in weight and cost. The incorporation of electronic components for the EOR controller, including a switch for reaching targeted O₂ concentration and a fixed resistor for O₂ removal rate regulation, enables multi-dimensional O₂ removal control. The system also realizes the O₂ concentration estimation in real-time with ±1% accuracy (within the 21%-1% range) by calculating electron transfers. The EOR controller's effectiveness is validated in plant hypoxia stress experiments, demonstrating precise O₂ level adjustments and its potential across various applications requiring controlled hypoxic conditions.

Wound healing is a complex process involving sequential stages of hemostasis, inflammation, proliferation, and remodeling. Multiple cell types and factors, including underlying conditions like diabetes and bacterial colonization, can influence healing outcomes and scar formation. N6-methyladenosine (m6A), a predominant RNA modification, plays crucial roles in gene expression regulation, impacting various biological processes and diseases. m6A regulates embryonic skin morphogenesis, wound repair, and pathophysiological processes like inflammation and angiogenesis. Recent studies have highlighted the role of m6A in wound healing, scar formation, and tissue remodeling. Additionally, m6A presents a unique expression pattern in pathological wounds and scars, potentially influencing wound healing and scar formation through modulating gene expression and cellular signaling, thereby serving as potential biomarkers or therapeutic targets. Targeting m6A modifications are potential strategies to enhance wound healing and reduce scar formation. This review aims to explore the roles and mechanisms of m6A RNA methylation in wound healing and scars, and discuss current challenges and perspectives. Continued research in this field will provide significant value for optimal wound repair and scar treatment.

Microglia, as immune cells in the central nervous system, possess the ability to adapt morphologically and functionally to their environment. Glymphatic system, the principal waste clearance system in the brain, exhibits circadian rhythms. However, the impact of microglia on the glymphatic system function remains unknown. In this study, we explored the intricate relationship between microglia and the glymphatic system. Examining diurnal patterns, we identified synchronized behaviors in glymphatic activity and microglial morphology, peaking during sleep and exhibiting distinct changes in branching complexity. Depleting microglia using PLX5622 or in P2Y12 knockout mice enhanced glymphatic function. Chemogenetic manipulation of microglia demonstrated that activating HM3D improved glymphatic function, while inhibiting HM4D unexpectedly increased microglial complexity. These findings highlight the dynamic influence of microglia on the glymphatic system.

Wound healing in diabetic patients is frequently hampered. Adipose-derived stem cell exosomes (ADSC-eoxs), serving as a crucial mode of intercellular communication, exhibit promising therapeutic roles in facilitating wound healing. This review aims to comprehensively outline the molecular mechanisms through which ADSC-eoxs enhance diabetic wound healing. We emphasize the biologically active molecules released by these exosomes and their involvement in signaling pathways associated with inflammation modulation, cellular proliferation, vascular neogenesis, and other pertinent processes. Additionally, the clinical application prospects of the reported ADSC-eoxs are also deliberated. A thorough understanding of these molecular mechanisms and potential applications is anticipated to furnish a theoretical groundwork for combating diabetic wound healing.