ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Macrophage-Derived Extracellular Vesicles Deliver Progranulin to Alleviate Skin Wound Fibrosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Optimal wound healing is crucial for patient recovery. Macrophage-fibroblast crosstalk is central to this process. Progranulin (PGRN) is involved in tissue repair, yet its intercellular transport and signaling mechanisms remain unclear. This study investigates how macrophage-derived PGRN, via extracellular vesicles (EVs), regulates fibroblast behavior during healing. Using murine scRNA-seq and transwell co-culture, we found that macrophages suppress fibroblast activation. Mechanistically, macrophage-derived PGRN was packaged into EVs and internalized by fibroblasts, upregulating DnaJ heat shock protein family member C3 (DNAJC3). Rescue experiments confirmed that DNAJC3 is essential for PGRN to inhibit the serum response factor (SRF)/alpha-smooth muscle actin (α-SMA)/connective tissue growth factor (CTGF) pathway. In a mouse wound model, PGRN-enriched EVs accelerated healing and improved healing quality, while EVs from Grn-silenced macrophages were less effective. We identify a novel EV-mediated pathway: macrophage PGRN targets fibroblast DNAJC3 to suppress fibrotic signaling. This reveals a fundamental regulatory mechanism and highlights macrophage EVs as promising natural therapeutics for fibrotic skin disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.