Evidence map›Paper›PMID 39865653›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025

CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.

Wooil Choi, Dong Jun Park, Robert A Dorschner, Keita Nakatsutsumi, Michelle Yi, Brian P Eliceiri

Abstract read
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In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Wooil ChoiDepartment of Surgery, University of California, San Diego, La Jolla, CA 92093, USA.
Dong Jun ParkDepartment of Surgery, University of California, San Diego, La Jolla, CA 92093, USA.
Robert A DorschnerDepartment of Dermatology, University of California, San Diego, La Jolla, CA 92093, USA.
Keita NakatsutsumiDepartment of Surgery, University of California, San Diego, La Jolla, CA 92093, USA.
Michelle YiDepartment of Surgery, University of California, San Diego, La Jolla, CA 92093, USA.
Brian P EliceiriDepartment of Surgery, University of California, San Diego, La Jolla, CA 92093, USA; Department of Dermatology, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: beliceiri@health.ucsd.edu.

Funding

UC San Diego Clinical and Translational Research InstituteKL2TR001444 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DEPP, COLIN A. · 2015 to 2024
$15.4M
Mechanisms of extracellular vesicle biogenesis that regulate wound healingR35GM149245 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Brian P Eliceiri · 2023 to 2026
$1.7M
NCATS NIH HHS KL2 TR001444NIGMS NIH HHS R35 GM149245
6 · The paper itself

Abstract

Small extracellular vesicles (sEVs) mediate intercellular signaling to coordinate the proliferation of cell types that promote re-epithelialization of skin following injury. Cyclin-dependent kinase 1 (CDK1) drives cell division and is a key regulator of entry to the cell cycle. To understand the potential of sEV-mediated delivery of CDK1 to reverse impaired wound healing, we generated CDK1-loaded sEVs (CDK1-sEVs) and evaluated their ability to mediate cell proliferation, re-epithelialization, and downstream signaling responses in the wound bed. We found that treatment of human keratinocytes with CDK1-sEVs increased phosphorylation of the CDK1 target, eukaryotic translation inhibition factor 4E-binding protein 1 (4E-BP1), and histone H3 within 24 h via AKT and ERK phosphorylation, driving increased proliferation and cell migration. Treatment of the wound bed of diabetic obese mice, a model of delayed wound healing, with a single dose of CDK1-sEVs accelerated wound closure, increased re-epithelialization, and promoted the proliferation of keratinocytes. These studies show that delivery of CDK1 by sEVs can stimulate selective and transient proliferation of cell types that increase re-epithelialization and promote proliferation of keratinocytes to accelerate wound healing.

Indexed as

CDC2 Protein KinaseCell CycleDiabetes Mellitus, ExperimentalExtracellular VesiclesObesityWound HealingAnimalsCell MovementCell ProliferationDisease Models, AnimalHumansKeratinocytesMiceMice, ObesePhosphorylationRe-EpithelializationCDC2 Protein KinaseCDK1cell proliferationcyclin-dependent kinase 1diabetic wound healingextracellular vesicleskin re-epithelialization

Identifiers

PMID39865653
PMCPMC11897770

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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.