Evidence map›Paper›PMID 36841937›Full record

ArticleAdvanced healthcare materials2023

Engineering Inflammation-Resistant Cartilage: Bridging Gene Therapy and Tissue Engineering.

Angela Bonato, Philipp Fisch, Simone Ponta, David Fercher, Mikko Manninen, Daniel Weber, Kari K Eklund, Goncalo Barreto, Marcy Zenobi-Wong

Open access · hybridAbstract read
In one paragraph

Article in Advanced healthcare materials, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Angela BonatoDepartment of Health Sciences and Technology, ETH Zürich, Zürich, 8093, Switzerland.ORCID 0000-0001-5991-2483
Philipp FischDepartment of Health Sciences and Technology, ETH Zürich, Zürich, 8093, Switzerland.ORCID 0000-0003-4384-6682
Simone PontaDepartment of Health Sciences and Technology, ETH Zürich, Zürich, 8093, Switzerland.
David FercherDepartment of Health Sciences and Technology, ETH Zürich, Zürich, 8093, Switzerland.
Mikko ManninenOrton Orthopedic Hospital Helsinki, Helsinki, 00280, Finland.ORCID 0000-0002-9681-8821
Daniel WeberDivision of Hand Surgery, University Children's Hospital, Zürich, 8032, Switzerland.
Kari K EklundOrton Orthopedic Hospital Helsinki, Helsinki, 00280, Finland.
Goncalo BarretoOrton Orthopedic Hospital Helsinki, Helsinki, 00280, Finland.ORCID 0000-0003-4444-9208
Marcy Zenobi-WongDepartment of Health Sciences and Technology, ETH Zürich, Zürich, 8093, Switzerland.ORCID 0000-0002-8522-9909
ETH Zurich · CHUniversity of Helsinki · FIInvalidisäätiö · FIUniversity Children's Hospital Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Articular cartilage defects caused by traumatic injury rarely heal spontaneously and predispose into post-traumatic osteoarthritis. In the current autologous cell-based treatments the regenerative process is often hampered by the poor regenerative capacity of adult cells and the inflammatory state of the injured joint. The lack of ideal treatment options for cartilage injuries motivated the authors to tissue engineer a cartilage tissue which would be more resistant to inflammation. A clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 knockout of TGF-β-activated kinase 1 (TAK1) gene in polydactyly chondrocytes provides multivalent protection against the signals that activate the pro-inflammatory and catabolic NF-κB pathway. The TAK1-KO chondrocytes encapsulate into a hyaluronan hydrogel deposit copious cartilage extracellular matrix proteins and facilitate integration onto native cartilage, even under proinflammatory conditions. Furthermore, when implanted in vivo, compared to WT fewer pro-inflammatory M1 macrophages invade the cartilage, likely due to the lower levels of cytokines secreted by the TAK1-KO polydactyly chondrocytes. The engineered cartilage thus represents a new paradigm-shift for the creation of more potent and functional tissues for use in regenerative medicine.

Indexed as

Cartilage, ArticularTissue EngineeringAdultChondrocytesGenetic TherapyHumansInflammationcartilage tissue engineeringgene editinginflammation

Identifiers

PMID36841937
PMCPMC11468558
OpenAlexW4322100228

What OpenQuestion holds

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LicenceCC BY-NC
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.