Evidence map›Paper›PMID 31409528›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019

Pharmacological and Genetic Inhibition of Caveolin-1 Promotes Epithelialization and Wound Closure.

Ivan Jozic, Andrew P Sawaya, Irena Pastar, Cheyanne R Head, Lulu L Wong, George D Glinos, Tongyu Cao Wikramanayake, Harold Brem, Robert S Kirsner, Marjana Tomic-Canic

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

32 citing papers in PubMed, 43 citations in OpenAlex.

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  12. Downregulation of Caveolae-Associated Proteins in Psoriasis: A Case Series Study.JID innovations : skin science from molecules to population health · 2024
    Article
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  17. The NIDDK Diabetic Foot Consortium.Journal of diabetes science and technology · 2023
    Article
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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

10 authors at 2 institutions in 1 country.

Ivan JozicWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Andrew P SawayaWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Irena PastarWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Cheyanne R HeadWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Lulu L WongWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
George D GlinosWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Tongyu Cao WikramanayakeWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Harold BremDivision of Wound Healing and Regenerative Medicine, Newark Beth Israel Medical Center, RWJBarnabas Health, Newark, NJ 07112, USA.
Robert S KirsnerWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Marjana Tomic-CanicWound Healing and Regenerative Medicine Research Program, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA; Cellular and Molecular Pharmacology Graduate Program in Biomedical Sciences, University of Miami Miller School of Medicine, Miami, FL, USA. Electronic address: mtcanic@med.miami.edu.
University of Miami · USNewark Beth Israel Medical Center · US

Funding

Developing strategies for effective debridement in patients for venous leg ulcersR01AR073614 · NIAMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KIRSNER, ROBERT SCOTT, TOMIC-CANIC, MARJANA · 2018 to 2023
$2.6M
Perforin-2: The role of a novel antimicrobial protein in diabetic foot ulcersR01NR015649 · NINR · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI STRBO, NATASA, TOMIC-CANIC, MARJANA · 2015 to 2019
$2.6M
University of Miami Clinical Research Unit of the Diabetic Foot ConsortiumU01DK119085 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI KIRSNER, ROBERT SCOTT, LEV-TOV, HADAR · 2018 to 2022
$1.8M
Micro-RNA Molecules as Regulators of Diabetic Wound HealingR01NR013881 · NINR · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI TOMIC-CANIC, MARJANA · 2012 to 2015
$1.7M
NIAMS NIH HHS R01 AR073614NIDDK NIH HHS U01 DK119085NINR NIH HHS R01 NR013881NINR NIH HHS R01 NR015649
6 · The paper itself

Abstract

Chronic wounds-including diabetic foot ulcers, venous leg ulcers, and pressure ulcers-represent a major health problem that demands an urgent solution and new therapies. Despite major burden to patients, health care professionals, and health care systems worldwide, there are no efficacious therapies approved for treatment of chronic wounds. One of the major obstacles in achieving wound closure in patients is the lack of epithelial migration. Here, we used multiple pre-clinical wound models to show that Caveolin-1 (Cav1) impedes healing and that targeting Cav1 accelerates wound closure. We found that Cav1 expression is significantly upregulated in wound edge biopsies of patients with non-healing wounds, confirming its healing-inhibitory role. Conversely, Cav1 was absent from the migrating epithelium and is downregulated in acutely healing wounds. Specifically, Cav1 interacted with membranous glucocorticoid receptor (mbGR) and epidermal growth factor receptor (EGFR) in a glucocorticoid-dependent manner to inhibit cutaneous healing. However, pharmacological disruption of caveolae by MβCD or CRISPR/Cas9-mediated Cav1 knockdown resulted in disruption of Cav1-mbGR and Cav1-EGFR complexes and promoted epithelialization and wound healing. Our data reveal a novel mechanism of inhibition of epithelialization and wound closure, providing a rationale for pharmacological targeting of Cav1 as potential therapy for patients with non-healing chronic wounds.

Indexed as

Caveolin 1Cell MovementDiabetic FootErbB ReceptorsGene ExpressionGene Expression RegulationGlucocorticoidsHumansKeratinocytesProtein BindingReceptors, GlucocorticoidRe-EpithelializationSignal TransductionSkinWound HealingCaveolin 1ErbB ReceptorsGlucocorticoidsReceptors, GlucocorticoidCaveolin-1chronic woundsdiabetic foot ulcersskin re-epithelializationwound healing

Identifiers

PMID31409528
PMCPMC6838864
OpenAlexW2966556657

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.