Titanium mesh exposure after cranioplasty is the most serious complication of this procedure. Although some clinical experience has been gradually accumulated over the years in the diagnosis and treatment of titanium mesh exposure, the treatment is often not standardized and it is difficult to achieve satisfactory repair results due to insufficient understanding of its pathogenesis and concurrent infections. To normalize the diagnosis and treatment of titanium mesh exposed wounds after cranioplasty and improve the therapeutic effect and the quality of life of patients, the Wound Repair Professional Committee of Chinese Medical Doctor Association organized an expert discussion based on the literature and current diagnosis and treatment status of titanium mesh exposed wounds after cranioplasty at home and abroad, and reached a consensus on the pathogenesis, preventive measures, and diagnosis and treatment strategies of titanium mesh exposed wounds after cranioplasty to provide reference for relevant clinicians.
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Open Access
Guideline
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Open Access
Review
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Sebaceous glands (SGs), as holocrine-secreting appendages, lubricate the skin and play a central role in the skin barrier. Large full-thickness skin defects cause overall architecture disruption and SG loss. However, an effective strategy for SG regeneration is lacking. Organoids are 3D multicellular structures that replicate key anatomical and functional characteristics of in vivo tissues and exhibit great potential in regenerative medicine. Recently, considerable progress has been made in developing reliable procedures for SG organoids and existing SG organoids recapitulate the main morphological, structural and functional features of their in vivo counterparts. Engineering approaches empower researchers to manipulate cell behaviors, the surrounding environment and cell–environment crosstalk within the culture system as needed. These techniques can be applied to the SG organoid culture system to generate functionally more competent SG organoids. This review aims to provide an overview of recent advancements in SG organoid engineering. It highlights some potential strategies for SG organoid functionalization that are promising to forge a platform for engineering vascularized, innervated, immune-interactive and lipogenic SG organoids. We anticipate that this review will not only contribute to improving our understanding of SG biology and regeneration but also facilitate the transition of the SG organoid from laboratory research to a feasible clinical application.
Open Access
Research Article
Issue
The spatiotemporal regulation of inflammatory dynamics is critical for successful wound healing. However, the precise mechanistic role of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome in orchestrating these processes remains incompletely characterized. This study aimed to delineate the specific mechanisms by which NLRP3 governs cellular and molecular events during wound healing.
Multi-omics sequencing data were utilized to profile NLRP3 inflammasome activation dynamics in murine and human acute wound models. Nlrp3−/− mice were generated using CRISPR-Cas9 technology. In vitro and in vivo functional assays were performed to assess NLRP3-dependent regulation of macrophage and fibroblast recruitment, polarization, and phenotype modulation.
NLRP3 is predominantly expressed in macrophages and neutrophils during the inflammatory phase of wound healing. Global deletion of Nlrp3 reduces IL-1β, the main downstream effector, attenuates CCL/CXCL chemokine signaling, decreases both inflammatory and pro-reparative cell infiltration, and disrupts the phenotypic switching of macrophages and fibroblasts, collectively delaying wound closure. However, the resulting low-inflammatory microenvironment in Nlrp3−/− mice may upregulate Wnt and Notch signaling early in the repair phase, curbing fibrosis and promoting appendage regeneration. Partial IL-1β blockade in WT mice recapitulates the NLRP3-null phenotype, whereas IL-1β reconstitution in knockout mice accelerates healing but increases fibrosis. Moreover, the NLRP3 protein also modulates fibroblast phenotype independently of inflammasome activation via a ROS-dependent mechanism.
NLRP3 exerts dual-phase regulatory roles in wound healing: (ⅰ) during inflammation, it drives chemokine-mediated macrophage/fibroblast recruitment and M1 polarization while suppressing fibroblast-mediated repair via IL-1β signaling; (ⅱ) later, NLRP3 deficiency enhances Wnt/Notch signaling, promoting structural restoration despite transiently delayed healing. Moreover, fibroblasts with high NLRP3 expression engage an inflammasome-independent NLRP3/ROS axis that augments activation of TGF-β/Smad signaling. These findings position NLRP3 as a potential therapeutic target for modulating phase-specific inflammatory and regenerative responses.
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