Evidence map›Paper›PMID 35077667›Full record

ArticleCell stem cell2022

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

Shamik Mascharak, Heather E Talbott, Michael Januszyk, Michelle Griffin, Kellen Chen, Michael F Davitt, Janos Demeter, Dominic Henn, Clark A Bonham, Deshka S Foster and 6 more

Abstract read
In one paragraph

Article in Cell stem cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

132 citing papers in PubMed.

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72 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors.

Shamik MascharakDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Heather E TalbottDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael JanuszykDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michelle GriffinDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kellen ChenDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael F DavittDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Janos DemeterBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Dominic HennDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Clark A BonhamDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Deshka S FosterDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Nancie MooneyBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ran ChengBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Peter K JacksonBaxter Laboratory, Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Derrick C WanDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Geoffrey C GurtnerDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: ggurtner@stanford.edu.
Michael T LongakerDepartment of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: longaker@stanford.edu.

Funding

Center for Dental, Oral, and Craniofacial Tissue and Organ Regeneration (C-DOCTOR)U24DE029463 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG, LOTZ, JEFFREY C. · 2020 to 2024
$29.5M
Irradiated head and neck cancer soft tissue reconstruction by fat transfer.R01DE027346 · NIDCR · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T, WAN, DERRICK · 2018 to 2022
$1.9M
Mechanoresponsive Engrailed-1-negative fibroblasts activate Engrailed-1 to promote fibrosis in wound healingR01GM136659 · NIGMS · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T · 2020 to 2023
$1.3M
Fibroblast lineage mechanisms of scarless skin healingR01GM116892 · NIGMS · STANFORD UNIVERSITY · PI LONGAKER, MICHAEL T, LORENZ, HERMANN PETER · 2017 to 2020
$1.2M
NIDCR NIH HHS R01 DE027346NIDCR NIH HHS U24 DE029463NIGMS NIH HHS R01 GM116892NIGMS NIH HHS R01 GM136659
6 · The paper itself

Abstract

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 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 mechanotransduction yields regenerative repair by fibroblasts with activated Trps1 and Wnt signaling. Finally, via 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 multi-omic map of wound regeneration and could have therapeutic implications for pathologic fibroses.

Indexed as

CicatrixWound HealingAnimalsFibroblastsFibrosisMechanotransduction, CellularMiceRepressor ProteinsSkinRepressor ProteinsTrps1 protein, mousefibroblast heterogeneityfibrosismechanotransduction signalingregenerationwound healing

Identifiers

PMID35077667
PMCPMC8988390

What OpenQuestion holds

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Registered trials

None linked

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.