Journal: Frontiers in Immunology

Article Title: Identification of MTURN as a trained immunity-related biomarker for heart failure via integrative transcriptomic machine learning analysis and experimental validation

doi: 10.3389/fimmu.2026.1739660

Figure Lengend Snippet: Identification of core genes associated with macrophage immune training and heart failure. (A) Schematic overview of human-derived macrophage trained immunity model and transcriptomic profiling workflow ( GSE235897 ). (B) The volcano plot and (C) DEGs heatmap of hMDMs from trained (n=3) and untrained (n=3) samples in the macrophage-trained immunity dataset GSE235897 (|log2FC| ≥ 0.585, p < 0.05). (D) Sample clustering dendrogram of GSE135055 dataset based on gene expression profiles. (E) Scale-free topology fit index and (F) mean connectivity analysis across a range of soft-thresholding powers. (G) Cluster dendrogram of genes showing co-expression modules identified by WGCNA in database GSE135055 . (H) Module-trait heatmap values represent correlation coefficients between healthy controls and HF samples (* p < 0.05, ** p < 0.01). (I) Venn diagram showing the overlap among heart failure DEGs, trained-immunity DEGs, and WGCNA module genes.

Article Snippet: For single-cell transcriptomic data, we accessed the SCP1303 project from the Broad Institute ( https://singlecell.broadinstitute.org/single_cell ), which includes raw scRNA-seq data from failing human hearts with dilated and hypertrophic cardiomyopathy.

Techniques: Derivative Assay, Gene Expression, Expressing

Journal: Frontiers in Immunology

Article Title: Identification of MTURN as a trained immunity-related biomarker for heart failure via integrative transcriptomic machine learning analysis and experimental validation

doi: 10.3389/fimmu.2026.1739660

Figure Lengend Snippet: Five heart failure transcriptomic datasets were integrated with a macrophage-trained immunity model to identify immune-related biomarkers. Through DEGs analysis, WGCNA, CIBERSORT, and six machine learning algorithms, hub genes were prioritized with MTURN emerging as the top candidate. Its potential was further validated by scRNA-seq analysis, which confirmed MTURN enrichment in cardiac macrophages. Finally, MTURN expression was validated using previously published heart failure transcriptomic data and in vitro experiments.

Article Snippet: For single-cell transcriptomic data, we accessed the SCP1303 project from the Broad Institute ( https://singlecell.broadinstitute.org/single_cell ), which includes raw scRNA-seq data from failing human hearts with dilated and hypertrophic cardiomyopathy.

Techniques: Expressing, In Vitro

Journal: eBioMedicine

Article Title: Multi-ancestry genome-wide association study of serum creatine kinase implicates myopathy genes and muscle pathways

doi: 10.1016/j.ebiom.2026.106274

Figure Lengend Snippet: Multi-ancestry genome-wide association and tissue/cell-type enrichment analyses. (A) Manhattan plot of multi-ancestry GWAS results for CK across all autosomes; the red dashed line denotes the genome-wide significance threshold (P = 5 × 10 −8 ). Previously unreported lead SNPs are shown in red; for clarity only previously unreported loci with exonic lead SNPs are annotated with mapped genes. The y axis is capped at −log 10 (P) = 50; peaks exceeding this value are truncated and marked with arrows, with lead variants and mapped genes rs7305678 (CD163/APOBEC1), rs11559024 (CKM), rs12975366 (LILRB5) and rs7481951 (ANO5). (B & C) MAGMA tissue and cell-type enrichment analysis based on (B) GTEx expression data, (C) Human Protein Atlas single-cell expression profiles; the dashed line indicates the Bonferroni-corrected significance threshold, and significant tissues and cell types are shown in red.

Article Snippet: Single-cell transcriptomic data from the Human Protein Atlas further supported these findings, showing significant enrichment in skeletal myocytes ( P = 4.39 × 10 −7 ) and cardiomyocytes ( P = 2.39 × 10 −4 ) among 81 evaluated cell types, with monocytes ranking third ( P = 3.23 × 10 −3 ), though not significant after multiple testing correction ( C; ).

Techniques: GWAS, Genome Wide, Expressing, Single Cell

Journal: Aging Cell

Article Title: The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

doi: 10.1111/acel.70431

Figure Lengend Snippet: Single‐cell transcriptome landscape in aging cohort. (A) UMAP visualization of cell‐type‐specific annotation among the aging cohort, showing 9 cell groups in different colors. (B) UMAP visualization of immune cell subpopulation annotation across different age groups, displaying 21 subpopulations in different colors. (C) The proportion of 21 different cell types across age groups.

Article Snippet: Single‐cell transcriptomic data from 56 healthy individuals aged from birth to over 90 years were acquired from the Shanghai Pudong Cohort ( NCT05206643 ) (Synapse: syn61609846) (Wang, Li, et al. ).

Techniques: Single Cell

Journal: Aging Cell

Article Title: The Immune Cell Atlas of “Longevity Molecular Tag”: Identification of Principal Immune Cell Subsets and Their Underlying Molecular Regulatory Mechanisms

doi: 10.1111/acel.70431

Figure Lengend Snippet: Centenarian phenotype‐associated immune cell type analysis at single‐cell resolution. (A) UMAP visualization of cell‐type‐specific annotation among immune cells, showing 9 cell groups in different colors. (B) UMAP visualization of subcellular annotation among immune cell subpopulations, showing 21 subpopulations in different colors. (C) UMAP visualization of Scissor + and Scissor − cells. (D, E) Proportional fractions of identified cell types across Scissor +/− conditions among extracted immune cells.

Article Snippet: Single‐cell transcriptomic data from 56 healthy individuals aged from birth to over 90 years were acquired from the Shanghai Pudong Cohort ( NCT05206643 ) (Synapse: syn61609846) (Wang, Li, et al. ).

Techniques: Single Cell

Journal: Signal Transduction and Targeted Therapy

Article Title: Parathyroid hormone–related protein is a therapeutic target in idiopathic pulmonary fibrosis

doi: 10.1038/s41392-026-02578-8

Figure Lengend Snippet: PTHrP expression in IPF and BLM-induced PF in humans. a Procedure for bioinformatics-based transcriptome analysis. b Identification of 714 commonly up- or downregulated genes in human IPF lungs using publicly available transcriptome datasets. c Top 9 activated gene sets identified by KEGG pathway analysis based on 714 common genes. d Identification of 5 genes through the intersection of genes related to soluble mediators, PTH synthesis, secretion, and action and 714 common genes. e Heatmap of PTHLH expression in normal and IPF samples. f PTHLH mRNA in normal and IPF samples. g Representative images of IF staining of PTHrP and quantification of the intensity of expression of PTHrP in human pulmonary interstitial fibrosis tissue microarrays from patients with IPF ( n = 23) and healthy donors ( n = 4). A magnified view of the region highlighted in the red box is shown. Scale bar: 50 μm and 100 μm (low magnification). a , b , d were created with BioRender.com. Data are shown as the mean ± SEM. P values were determined by two-tailed Student’s t test ( f , g ). *** P < 0.001

Article Snippet: To confirm the predominance of tissue-specific expression of PTHLH in human tissues, we reanalyzed publicly available single-cell transcriptome data provided by The Human Protein Atlas.

Techniques: Expressing, Staining, Two Tailed Test

Journal: Cellular Oncology (Dordrecht, Netherlands)

Article Title: Platelets in the tumor microenvironment: potential mediators of immune exclusion and resistance to immune checkpoint inhibitor therapy

doi: 10.1007/s13402-025-01129-7

Figure Lengend Snippet: Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

Article Snippet: Our analysis of pan-tissue single-cell transcriptomic data from the Human Protein Atlas identifies platelets as a dominant cellular source of TGF-β and among the highest expressors of PDGFB across human cell types (Fig. A), providing a strong molecular basis for their impact on CAF activation and differentiation.

Techniques: Activation Assay, Expressing, RNA Sequencing, Derivative Assay