Naftali Kaminski

This study identifies a monocyte-macrophage-fibroblast axis in post-COVID-19 lung fibrosis using multi-omic profiling and shows its potential as a therapeutic target.

This study shows that sobetirome, a thyroid hormone receptor beta agonist, reduces pulmonary fibrosis in mice and human tissue by restoring mitochondrial function and modulating apoptosis.

This study shows that the TGF-β1/mTORC1 signalling axis regulates the transcriptional identity of CTHRC1+ fibroblasts in IPF, supporting mTORC1 as a therapeutic target.

This study uses single-cell and spatial transcriptomics to identify structural cell circuits in BOS lungs and their spatial organization during airway obliteration.

This study identifies aberrant cell populations in RAS lungs using snRNA-seq and histology, revealing a fibrotic niche composed of specific cell types with potential therapeutic targets.

SPEAK identifies spatial domains in spatial transcriptomics data using a large language model and expert-aligned prompts, showing improved accuracy and interpretability.

This paper identifies compartment- and cell-specific molecular programs in preclinical familial pulmonary fibrosis using multi-omic profiling and finds these signatures are partially represented in peripheral blood.

TLR5 deficiency is linked to pulmonary fibrosis due to its role in preventing microbial dysbiosis following lung injury.

This study identifies early alveolar niche disruption and aberrant epithelial reprogramming in IPF using multi-modal analyses of patient cohorts.

This study identifies three novel genetic signals associated with idiopathic pulmonary fibrosis using GWAS and clinically-curated datasets, highlighting potential drug targets like MUC1 and NTN4.

This paper presents the first single-nucleus RNA sequencing atlas of pleuroparenchymal fibroelastosis, identifying novel cell states and their spatial organization in lung fibrosis.

This study identifies pro-inflammatory monocyte and macrophage subsets driven by lupus immune complexes, independent of type I interferon signaling, using scRNA-seq and proteomic analysis.

This study identifies VEGF-D as a key factor in maintaining lung vascular integrity during acute lung injury using single-cell RNA sequencing and functional assays.

This study performs GWAS of IPF using dominant and recessive models, identifying five new genome-wide significant signals and genes, including PMF1 and EPN3, and observing increased PMF1 expression in IPF patients.

This study evaluates modified RNA extraction methods to remove agarose impurities from precision-cut lung slices, showing improved RNA quantity and integrity using a plant kit and agarose dissolution.

The paper investigates age-related changes in proximal pulmonary artery mechanics in mouse models, finding increased stiffness and collagen reorientation linked to aging biomarkers and cellular senescence.

This study characterizes epithelial cell states emerging from reprogramming in a pulmonary bioengineering context.

This study uses spatial transcriptomics to identify hybrid pro-inflammatory and pro-fibrotic cellular niches in sarcoidosis granulomas, linking them to fibrosis and immune responses.

This study creates a spatial transcriptomics atlas of human tuberculosis and non-tuberculous mycobacterial granulomas, identifying distinct niches and immune signatures.

The paper identifies transcriptional programs in fibroblastic foci fibroblasts using spatial and single-cell transcriptomics, revealing MMP11 as a prognostic biomarker and potential therapeutic target.

The paper uses single-cell transcriptomics to analyze an IPF cohort, revealing a transcriptional deficit refractory to current treatments and identifying STAT3 as a key regulator in the therapeutic gap.

Single-nucleus multiomic and ex vivo lung slice profiling of human idiopathic pulmonary fibrosis identifies Alveolar Intermediate cells bridging alveolar and Aberrant Basaloid states and reveals AP-1 chromatin injury memory.

This study introduces two RTEL1 mouse models with distinct mutations at amino acid 492, showing that M492K affects telomere length while M492I impairs telomere protection, leading to different disease phenotypes.

This study uses single-cell RNA sequencing to analyze sputum cells from asthma patients and controls, identifying dysregulated pathways and communication networks involved in asthma pathogenesis.

This study identifies CD103+ dendritic cell-fibroblast crosstalk via TLR9 and AHR signaling as a driver of lung fibrosis in IPF, showing that inhibiting AHR signaling reduces fibrosis.

This study examines hypoxia-induced cardiopulmonary remodeling in mice, finding that pulmonary artery stiffening due to collagen remodeling precedes and correlates with cardiac and lung dysfunction, with partial recovery observed after normoxia.

This study investigates GPR87's role in pulmonary fibrosis, finding it highly expressed in IPF lungs and protective against fibrosis when knocked down in multiple models.

This study develops an engineered whole-lung tissue model to study tissue organization and alveolar barrier function, showing improved barrier function with alveolar macrophages.

The paper identifies dedifferentiated early postnatal lung myofibroblasts that persist into adulthood and redifferentiate in response to injury.

This study identifies three genetic variants with sex-specific effects on IPF susceptibility but finds no significant difference in predictive accuracy of polygenic risk scores between males and females.