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Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [Spatial transcriptomics]

ABSTRACT: Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [Spatial transcriptomics]

PROVIDER: PRJNA1165793 | ENA |

REPOSITORIES: ENA

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Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis

Project description:Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis

| PRJNA1165197 | ENA

Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [scATAC-seq]

Project description:Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [scATAC-seq]

| PRJNA1165329 | ENA

Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis

Project description:In the skin, tissue injury results in fibrosis in the form of scars composed of dense extracellular matrix deposited by fibroblasts. The therapeutic goal of regenerative wound healing has remained elusive, in part because principles of fibroblast programming and adaptive response to injury remain incompletely understood. Here, we present a multimodal -omics platform for the comprehensive study of cell populations in complex tissue, which has allowed us to characterize the cells involved in wound healing using a bleomycin induced ifibrosis model. We employ a bleomycin skin models that recapitulates human tissue repair kinetics. Through integrated analysis of single cell chromatin landscapes and gene expression states, coupled with spatial transcriptomic profiling, we are able to impute fibroblast epigenomes with temporospatial resolution. This has allowed us to reveal potential mechanisms controlling fibroblast fate during migration, proliferation, and differentiation following skin injury, and thereby reexamine the canonical phases of wound healing. These findings have broad implications for the study of tissue repair in complex organ systems.

2025-08-13 | GSE277998 | GEO

Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [Spatial transcriptomics]

2025-08-13 | GSE278169 | GEO

Multi-omic analysis reveals retinoic acid molecular drivers for fibrosis and regenerative repair in skin fibrosis [scATAC-seq]

2025-08-13 | GSE278069 | GEO

Multi-omic analysis reveals retinoic acid molecular drivers for dermal fibrosis and regenerative repair in the skin.

Project description: Not available

| S-EPMC12373384 | biostudies-literature

Multi-omic analysis reveals divergent molecular events in scarring and regenerative wound healing

Project description:Regeneration is the “holy grail” of tissue repair, but skin injury typically yields fibrotic, non-functional scars. Developing pro-regenerative therapies requires rigorous understanding of the molecular progression from injury to fibrosis or regeneration. Here, we report the divergent molecular events driving skin wound cells toward either scarring or regenerative fates. We profile scarring versus YAP inhibition-induced wound regeneration at the transcriptional (single-cell RNA-sequencing), protein (timsTOF proteomics), and tissue (extracellular matrix ultrastructural analysis) levels. Using cell surface barcoding, we integrate these data to reveal fibrotic and regenerative “molecular trajectories” of healing. We show that disrupting YAP mechanical signaling yields regenerative repair orchestrated by fibroblasts with activated Trps1 and Wnt signaling. Finally, by performing in vivo gene knockdown and overexpression in wounds, we identify Trps1 as a key regulatory gene that is necessary and partially sufficient for wound regeneration. Our findings serve as a multimodal map of wound regeneration and could have therapeutic implications for pathologic fibroses.

2022-01-24 | GSE186527 | GEO

Egr1 regulates regenerative senescence and cardiac repair

Project description:Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA-sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and Agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, Agrin-induced senescence and repair require Egr1, activated by the integrin/FAK-ERK/Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype (SASP) components that promote ECM degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process.

2024-05-07 | GSE253383 | GEO

Multi-omic analysis reveals divergent molecular events in scarring and regenerative wound healing

Project description:Multi-omic analysis reveals divergent molecular events in scarring and regenerative wound healing

| PRJNA774283 | ENA

Egr1 is a master regulator of regenerative senescence and cardiac repair

2024-05-06 | GSE255181 | GEO