Dong L, et al. World J Mens Health. 2021 Oct;39(4):776-796. https://doi.org/10.5534/wjmh.200155

The skin surface is colonised by a rich microbiome, and intricate interactions between this microenvironment and microbial communities are critical for maintaining skin homeostasis. Atopic dermatitis (AD), a chronic inflammatory skin disease characterised by skin barrier dysfunction and aberrant immune activation, exhibits a rising global incidence. While conventional therapeutic strategies offer short-term symptom control, their long-term use is limited by adverse effects including skin atrophy, metabolic disorders, and increased infection risk. Critically, these approaches fail to cure AD or reverse the underlying immune imbalance. Recent research has firmly established the skin microbiome as a central driver in AD pathogenesis. The molecular mechanisms underpinning microbiome-host interactions, including the potential for remote regulation via the gut-skin axis, are now being actively investigated. This review systematically analyses how microbial dysbiosis in AD promotes Th2/Th17 immune polarization through three key pathways: microbial metabolites, immune signalling, and barrier integrity. Building on these mechanistic insights and recent advances, we propose novel multimodal therapeutic strategies targeting the microbial-immune axis. We further elucidate the role of commensal bacteria in maintaining immune homeostasis. Ultimately, this synthesis aims to bridge fundamental research with clinical applications, providing a robust theoretical foundation for future therapeutic development and clinical studies in AD management.

N6-methyladenosine (m6A) modification is a pivotal mechanism in RNA epigenetics, with profound implications for lung cancer (LC) biology. This review synthesizes current knowledge on m6A’s multifaceted regulatory networks in non-small cell lung cancer (NSCLC), elucidating its roles in tumor proliferation, apoptosis, invasion, and metastasis. We further explore how m6A governs metabolic reprogramming—including glycolysis and ferroptosis—angiogenesis, and tumor microenvironment (TME) remodeling. Additionally, m6A-mediated modification of non-coding RNAs contributes to LC malignancy, underscoring its potential as a diagnostic and prognostic biomarker. These findings also offer novel strategies to overcome therapeutic resistance, a critical challenge in NSCLC treatment. Despite its promise, clinical translation of m6A-targeted interventions faces hurdles, such as the lack of standardized detection methods, the complexity of m6A-associated regulatory networks, and unresolved crosstalk with other RNA modifications. Future research should prioritize multi-omics approaches to resolve these challenges and advance m6A from mechanistic discovery toward clinical application. By addressing these gaps, m6A modulation may emerge as a transformative avenue in precision oncology.

Background: Depression is a major global health challenge, and traditional cognitive behavioral therapy (CBT) is constrained by therapist shortages and economic barriers. CBT-based mobile applications offer a scalable and accessible alternative, yet a comprehensive overview of their global research landscape remains limited. Objective: To map global research trends, clinical progress, and emerging frontiers in CBT-based mobile applications for depression using bibliometric methods. Methods: Relevant studies were systematically retrieved from the Web of Science Core Collection, PubMed, and PsycINFO from inception to June 25, 2025. CiteSpace 6.4 R1, Microsoft Excel 2019, and Python were used for visualization and data analysis, including temporal publication trends, co-authorship, co-citation, keyword analyses, and citation burst detection. Results: The WoSCC analysis identified 350 articles published between 2013 and 2025, showing a marked growth trajectory with leading contributions from the United States and major academic centers. Dominant themes included smartphone interventions, blended treatments, CBT for insomnia, and adolescent depression, while citation bursts indicated recent shifts toward prevention, technology integration, and standardized outcome measures. The PubMed analysis included 72 clinical trial articles, highlighting randomized controlled trials as the predominant design and revealing growing interest in integrating interpersonal therapy and mindfulness within broader, interdisciplinary treatment frameworks. The PsycINFO analysis comprised 20 articles and provided a complementary behavioral science perspective, emphasizing mobile phone–delivered CBT for major depression, digital interventions targeting comorbid social anxiety, culturally adapted applications for Chinese cultural groups, and emerging work linking mobile health and virtual reality. Conclusions: Research on CBT-based mobile applications for depression is rapidly advancing toward more personalized, adaptive, and preventive digital interventions grounded in robust clinical and behavioral evidence. Strengthening global, interdisciplinary collaboration and leveraging innovative technologies will be critical for translating these tools into effective, scalable services. Over the next 5–10 years, key research streams are likely to include the integration of Artificial Intelligence (AI) and large language models (LLMs) into mobile CBT platforms and the convergence of app-based interventions with sensor-based digital phenotyping, wearable devices, and immersive technologies to enhance real-time monitoring, user engagement, and long-term outcomes, with the potential to narrow treatment gaps across diverse populations. Systematic review registration: https://osf.io/ , Identifier: https://doi.org/10.17605/OSF.IO/YCSR8 .

Tumor-associated macrophages (TAMs) within the tumor microenvironment (TME) play a central role in tumor progression and therapeutic resistance in gynecological malignancies, including ovarian cancer (OC), cervical cancer (CC), and endometrial cancer (EC). This review systematically summarizes common regulatory mechanisms and tumor-specific variations in TAMs across these three malignancies, emphasizing the dual-origin developmental trajectories of tissue-resident macrophages and monocyte-derived macrophages, the CCL2-CCR2 and CSF1-CSF1R core signaling axes, and the regulation of TAMs’ functional polarization by hypoxia and metabolic reprogramming. Furthermore, the molecular mechanisms through which TAMs mediate immunosuppression and therapeutic resistance via physical barrier construction, metabolic competition, and antigen presentation impairment are analyzed, and the specific characteristics of the peritoneal microenvironment in OC, HPV-driven mechanisms in CC, and hormonal regulation in EC are compared. Therapeutic strategies targeting TAM recruitment, survival, and phenotypic reprogramming are discussed, along with TAM markers, and may provide a theoretical foundation and clinical indications for overcoming immune therapeutic resistance in gynecological malignancies.

Breast cancer is among the most common forms of cancer in women worldwide and continues to be a major challenge in medical science and clinical care because of the complexity of its biological nature and common resistance to treatment. Nanoparticles for treating breast cancer are becoming a new-generation approach to induce the death of breast cancer cells because of their favorable physicochemical properties and excellent targeting ability. Recent studies have shown that nanoparticles can significantly increase anticancer activity by activating several cell death mechanisms, such as pyroptosis, apoptosis, necroptosis, autophagy, ferroptosis, cuproptosis, and disulfidptosis. The present review focuses on the molecular processes that lead to cell death in breast cancer models due to nanoparticle exposure. Such mechanisms have also been documented in other solid tumors, suggesting the possible universality of the cell death induced by nanoparticles. In the current review, we systematically summarize the molecular mechanisms underlying the various forms of cell death caused by nanoparticles in breast cancer cells to provide a theoretical background for the translational use of nanotechnology in precise breast cancer treatment and a cross-validation model for future mechanistic research on various types of cancer.