Ran Huo

Infantile hemangioma (IH) is the most common benign tumor of infancy. Hypoxia and activation of hypoxia-inducible factor (HIF) signaling have been proposed to contribute to IH pathogenesis, yet the role of endothelial PAS domain-containing protein 1 ( EPAS1 ), which encodes hypoxia-inducible factor-2α (HIF-2α), in hemangioma endothelial cells (HemECs) remains less well characterized. Here, we investigated HIF-2α in primary HemECs using a pharmacological inhibitor (PT-2399) and shRNA-mediated EPAS1 knockdown under normoxic and hypoxic conditions. In hypoxic cultures, PT-2399 treatment was associated with reduced migration and invasion and with a reduction in junction number in tube formation assays; at the selected dose, PT-2399 did not significantly reduce cell viability. By contrast, EPAS1 knockdown was associated with reduced proliferative capacity and altered cell cycle distribution, together with enrichment of DNA replication/cell cycle-related transcriptional programs, negative enrichment of MYC- and E2F-related gene sets, and directionally consistent protein level changes in selected regulators. EPAS1 knockdown-associated phenotypic trends were broadly similar under normoxia and hypoxia, with no clear evidence that hypoxic stimulation enhanced the magnitude of these changes. In IH tissue transcriptomic data, Egl-9 family hypoxia-inducible factor 3 ( EGLN3 ) showed reduced expression, consistent with a testable hypothesis that hypoxia-independent mechanisms may contribute to maintenance of HIF-2α activity in this context. This study is limited by the use of HemECs derived from a single IH specimen and by the absence of on-target validation; accordingly, the findings should be interpreted as exploratory and hypothesis-generating.

Muir-Torre syndrome (MTS) is an uncommon autosomal dominant disorder characterized by germline mutations in DNA mismatch repair (MMR) genes, resulting in microsatellite instability (MSI). It is regarded as a variant form of Lynch syndrome, characterized by the co-occurrence of at least one cutaneous sebaceous neoplasm and at least one visceral malignancy. Furthermore, studies have indicated that MTS may manifest in transplant recipients and in immunocompromised patients. The diagnosis and management of such cases necessitate a multidisciplinary approach. Here, we report a case of a Chinese patient with a history of rectal cancer who developed multiple sebaceous adenomas during immunosuppressive therapy six years after renal transplantation. This case report not only provides additional evidence for the inducing effect of immunosuppressants on MTS but also emphasizes the importance of a thorough diagnosis of MTS and the significance of preventing the development of potential skin tumors in patients with MTS.

Progressive hemifacial atrophy (PHA) is a progressive, irreversible disorder characterized by unilateral facial soft tissue atrophy. Conventional treatments, such as isolated fat grafting or synthetic fillers, are often limited by high resorption rates and insufficient structural support. To address these challenges, a staged surgical protocol integrating autologous fat grafting (AFG) and autologous dermal grafting was implemented to optimize outcomes in moderate-to-severe cases. This study evaluates the synergistic efficacy of combined AFG and dermal grafting in the treatment of PHA. Two patients underwent sequential procedures: initial AFG using the Coleman technique with abdominal fat harvest, followed by dermal grafting from the gluteal region to address residual deep depressions. Postoperative evaluations, including long-term follow-up (up to 20 months), assessed volumetric retention, complications, and patient satisfaction. Results demonstrated significant improvements in facial symmetry and contour, with dermal grafts providing durable structural reinforcement in areas where fat resorption persisted. No major complications were observed, and both patients reported high satisfaction with aesthetic outcomes. The staged integration of AFG and dermal grafting offers a minimally invasive, biocompatible solution for complex PHA reconstruction, leveraging dynamic adaptability and natural tissue integration. This dual-modality approach presents a promising strategy for recalcitrant soft tissue defects, particularly where traditional fat grafting alone proves insufficient.

Background: Stem cell exhaustion and cellular senescence are two hallmarks of aging. Mesenchymal stem cells (MSCs), as key players in tissue regeneration, are particularly vulnerable to senescence, which compromises both their endogenous regenerative capacity and their therapeutic efficacy in cell-based applications. Suppressing MSC senescence is therefore essential for developing effective regenerative and anti-aging strategies. Methods: We developed a serum-free adipose-conditioned medium (SF-ACM) from in vitro–cultured human adipose explants. Its anti-aging effects were evaluated in oxidative stress–induced and replicative senescence models of human adipose-derived stem cells (ADSCs), assessing proliferation, senescence markers, migration, and trilineage differentiation. Parallel experiments in senescent human dermal fibroblasts (HDFs) examined proliferation, fibrosis, and senescence features. In vivo, male C57BL/6 J mice (4 or 16 months old) with D-galactose–induced and naturally aged mice received intraperitoneal SF-ACM. Aging phenotypes were analyzed in skin, adipose tissue, muscle, kidney, and serum, along with hepatic and renal safety assessments. Results: SF-ACM significantly reduced senescence-associated markers, including p16, p21, p53, and SA-β-gal, enhanced Lamin B1 expression, and improved the proliferation, migration, and differentiation capacities of ADSCs. It also decreased senescence and fibrosis-related markers in HDFs. In aging mice, SF-ACM improved aging-associated phenotypes in skin, adipose tissue, and skeletal muscle. Mechanistically, these effects were associated with suppression of the IL-6/STAT3 signaling pathway. Conclusions: This study identifies a novel xenogeneic-free, paracrine-rich formulation that delays cellular senescence and preserves tissue homeostasis. These findings support its potential as a safe and effective strategy to suppress cellular aging, restore stem cell function, and ameliorate tissue-level aging, offering translational promise for regenerative medicine and anti-aging interventions.

Purpose: To investigate the role of myosin 1b (Myo1b) in infantile hemangiomas (IHs). Patients and Methods: The expression of Myo1b in IHs and normal skin tissues was evaluated using immunohistochemical techniques. Expression of Myo1b in hemangioma endothelial cells (HemECs) was detected using quantitative real-time polymerase chain reaction and Western blotting techniques. The effects of Myo1b on cell proliferation, invasion, tube formation and other biological characteristics were analyzed. A mouse model was established to observe the inhibitory effects of Myo1b in vivo. Protein expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and glucose transporter 1 protein (Glut-1) in a Myo1b knockdown HemECs was detected using Western blot. Results: Myo1b was highly expressed in the proliferative stage of IHs, and promoted proliferation, invasion, and angiogenesis in vitro. Mouse models further demonstrated that Myo1b inhibited proliferation and angiogenesis of IHs. Knockdown of Myo1b inhibited Glut-1 activity, promoted expression of PPARγ transcription factor. Conclusion: Myo1b has a pro-tumor effect on IHs, knockdown of Myo1b facilitated progression of the proliferating to involution phase of IHs. Therefore, Myo1b is expected to serve as a new target for the treatment of IHs.

Background: Despite numerous studies over the past two decades, clinical treatment for port wine stains (PWS) has shown limited progress. Analyzing evolutionary trends and research focal points can illuminate current deficiencies and guide future investigations. We aim to conduct a scientometric analysis and meta‐analysis to uncover the historical trajectory, research hotspots, and future directions of PWS. Methods: We conducted a scientometric analysis of articles related to PWS published between 2000 and 2023. Data were retrieved from the Web of Science Core Collection (WoSCC) and analyzed using R software, VOSviewer, and CiteSpace. Furthermore, we retrieved articles reporting therapeutic clearance rates for PWS from PubMed, Embase, Web of Science, and Cochrane search engines. A meta‐analysis was performed using Stata/MP to assess whether treatment outcomes for PWS have improved in the 21st century. Results: The annual scientific output was stable from 2000 to 2023. The top three countries in terms of document production were the United States, China, and the United Kingdom. Pulsed dye laser (PDL) and photodynamic therapy (PDT) were the two primary modalities used in the treatment of PWS. A notable difference exists in the preference for these treatment modalities between China and Western countries. The meta‐analysis shows improvement in treatment outcomes for PWS from 2000 to 2023. Conclusions: Although limited, treatment outcomes for PWS have shown improvement in the 21st century. However, there is a critical need for research directions that could revolutionize current treatment practices. Genetic discoveries have suggested promising therapeutic targets for potential breakthroughs in the future.

Plexiform neurofibromas (PNFs) are benign tumors that affect 20‑50% of patients with type I neurofibromatosis (NF1). PNF carries a risk of malignancy. There is no effective cure for PNF. Its onset may be associated with genetic and metabolic abnormalities, but the exact mechanisms remain unclear. Succinate‑CoA ligase GDP/ADP‑Forming Subunit α(SUCLG1), a catalytic enzyme in the tricarboxylic acid cycle, is highly expressed in PNF. The present study aimed to explore the role of SUCLG1 in function and metabolism of PNF cells. SUCLG1 expression was verified using western blotting and immunofluorescence. After inducing SUCLG1 knockdown and overexpression, functional changes in PNF cells were assessed, as well as effects of SUCLG1 on cell respiration and glucose metabolism. Quantitative PCR, WB, electron microscopy and Flow cytometry demonstrated that SUCLG1 enhanced mitochondrial quality and promoted mitochondrial fusion, thereby driving proliferation and migration of tumor cells, inhibiting apoptosis and altering the cell cycle. A Seahorse assay showed that elevated SUCLG1 expression enhanced cell aerobic respiration without affecting the glycolytic process. This suggests that SUCLG1 upregulation in PNF does not trigger the Warburg effect associated with malignant tumors. This study also demonstrated the positive regulation of cellular function by promoting the expression level of the SLC25A1 gene when SUCLG1 expression was elevated. In conclusion, SUCLG1 altered the mechanism of mitochondrial quality control to enhance cell aerobic respiration, thereby driving the pathogenesis of PNF. Thus, SUCLG1 can serve as a potential target in future therapeutic strategies.

Introduction: Scalp arteriovenous fistula (AVF) is a rare and intricate vascular anomaly characterized by a direct connection between an artery and a vein, without an intervening capillary system. This anomaly can induce significant local hemodynamic changes and is associated with various complications, such as pain, a pulsatile mass, increasing swelling, and venous hypertension skin ulcerations which may be non-healing. This study aimed to evaluate the efficacy and safety of interventional embolization treatments for scalp AVF at Shandong Provincial Hospital.Methods: This retrospective clinical analysis assessed 21 patients who underwent interventional embolization between 2018 and 2024. Patients included were those treated in the vascular surgery department at Shandong Provincial Hospital, who had comprehensive medical records and follow-up data. Treatment methods, outcomes, and complications were thoroughly analyzed through patient medical records.Results: Among the patients studied, direct puncture was the most prevalent treatment method, employed in 42.86% (9/21) of cases, followed by various combinations of arterial, venous, and direct approaches. Ethanol, used in 85.71% (18/21) of the cases, demonstrated its broad efficacy and application in clinical settings. Immediate imaging post-treatment confirmed a cure rate of 85.71% (18/21). The main postoperative complications included swelling, with some patients also experiencing nodules, scabbing, or hair loss.Conclusion: Interventional embolization has proven to be a safe and effective method for managing scalp AVF, significantly minimizing complications. Future research should focus on further optimizing these treatment methods to enhance efficacy and improve patient quality of life.