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Digitally Adapting LGBTQ-Affirmative Cognitive Behavioral Therapy for Chinese Men Who Have Sex With Men Living With HIV: User-Centered Design Approach
MedRoundsQA: A Persona and Difficulty Aware Evaluation for Multi-Turn Medical Consultations
Show-Harness: Just a VLM Agent Can Play Robots
Towards trustworthy agentic AI: a comprehensive survey of safety, robustness, privacy, and system security
LC-ERD: Mining Latent Logic for Self-Evolving Reasoning via Consistency-Regulated Reward Decomposition
SimuWoB: Simulating Real-World Mobile Apps for Fast and Faithful GUI Agent Benchmarking
MobileGym: A Verifiable and Highly Parallel Simulation Platform for Mobile GUI Agent Research
Unlocking the Potential of Continual Model Merging: An ODE Perspective
AnyMo: Geometry-Aware Setup-Agnostic Modeling of Human Motion in the Wild
Molecular basis for methylation-sensitive editing by Cas9
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10384-z
ThermoCas9, a genome-editing enzyme that is sensitive to the DNA methylation status of the target locus, is characterized and shows promise for targeting hypomethylated DNA regions in cancer cells.EBV strain interacts with host HLA to drive nasopharyngeal carcinoma risk
Nature, Published online: 15 April 2026; doi:10.1038/s41586-026-10416-8
A genome-to-genome association study identifies host and viral risk factors that interact to drive nasopharyngeal carcinoma endemicity in southern China.Transplantation of encapsulated mitochondria alleviates dysfunction in mitochondrial and Parkinson’s disease models
Beyond Static Vision: Scene Dynamic Field Unlocks Intuitive Physics Understanding in Multi-modal Large Language Models
DP-OPD: Differentially Private On-Policy Distillation for Language Models
Parallel Universes, Parallel Languages: A Comprehensive Study on LLM-based Multilingual Counterfactual Example Generation
Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.
ABSTRACT
Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.
PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094
Decoding macrophage heterogeneity in the pulmonary fibrosis lung cancer transition
Front Immunol. 2026 Mar 20;17:1787094. doi: 10.3389/fimmu.2026.1787094. eCollection 2026.
ABSTRACT
Pulmonary fibrosis (PF) significantly increases the risk of lung cancer (LC), but the mechanisms underlying this transition remain unclear. This overview positions macrophage heterogeneity as a central node within the PF-LC continuum. First, we describe important subpopulations of profibrotic and pro-tumor macrophages, including SPP1+, MERTK+, TREM2+, and MARCO+ cells, using high-resolution spatial and single-cell omics technologies. Next, we analyze the fundamental mechanisms that determine their function: the fibrotic microenvironment (e.g., extracellular matrix stiffness, hypoxia) induces profound metabolic reprogramming (e.g., Warburg effect, lipid peroxidation) and stabilizes epigenetic memory (e.g., DNA methylation, histone modifications), locking them into a pathogenic state. This reprogramming occurs through two main pathways: (1) metabolic reprogramming, characterized by aerobic glycolytic conversion and dysregulated lipid metabolism, which stimulates both pathogenic functions and suppression of T cell activity; (2) Epigenetic modifications, including stabilized alterations in DNA methylation, histone modifications, and superactivator patterns, which maintain cells in a tumor-promoting phenotype. As central nodes of communication, these macrophages interact pathologically with fibroblasts and epithelial cells through secreted factors and extracellular vesicles, forming self-reinforcing feedback loops that promote disease progression. We are studying the crucial role of new technologies, particularly multi-omic spatial models and high-precision organoids, in fostering mechanistic discoveries. These discoveries pave the way for new macrophage-focused therapeutic strategies, including the precise stratification of patients using biomarkers from liquid biopsies (such as soluble SPP1 and MARCO) and the development of targeted drug delivery systems for the selective modulation of macrophage function, thus establishing a new paradigm for therapeutic interventions in pulmonary fibrosis with concomitant lung cancer.
PMID:41939908 | PMC:PMC13046558 | DOI:10.3389/fimmu.2026.1787094