Evidence map›Paper›PMID 36552796›Full record

ReviewCells2022

Chondrocyte Hypertrophy in Osteoarthritis: Mechanistic Studies and Models for the Identification of New Therapeutic Strategies.

Shikha Chawla, Andrea Mainardi, Nilotpal Majumder, Laura Dönges, Bhupendra Kumar, Paola Occhetta, Ivan Martin, Christian Egloff, Sourabh Ghosh, Amitabha Bandyopadhyay and 1 more

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
10.0field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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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

11 authors at 5 institutions in 4 countries.

Shikha ChawlaDepartment of Surgery, Faculty of Medicine and Health Sciences, Research Institute of the McGill University Health Centre, Montreal, QC H3G 1A4, Canada.
Andrea MainardiDepartment of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.
Nilotpal MajumderRegenerative Engineering Laboratory, Department of Textile and Fibre Engineering, Indian Institute of Technology Delhi, Delhi 110016, India.
Laura DöngesDepartment of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.
Bhupendra KumarDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, Uttar Pradesh, India.
Paola OcchettaDepartment of Electronics, Information and Bioengineering, Politecnico di Milano, 20133 Milano, Italy.ORCID 0000-0002-5758-2019
Ivan MartinDepartment of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0001-6493-0432
Christian EgloffDepartment of Orthopaedic Surgery and Traumatology, University Hospital Basel, 4031 Basel, Switzerland.
Sourabh GhoshRegenerative Engineering Laboratory, Department of Textile and Fibre Engineering, Indian Institute of Technology Delhi, Delhi 110016, India.
Amitabha BandyopadhyayDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology Kanpur, Kanpur 208016, Uttar Pradesh, India.
Andrea BarberoDepartment of Biomedicine, University Hospital Basel, University of Basel, 4031 Basel, Switzerland.ORCID 0000-0001-5252-789X
University of Basel · CHIndian Institute of Technology Delhi · INIndian Institute of Technology Kanpur · INPolitecnico di Milano · ITUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Articular cartilage shows limited self-healing ability owing to its low cellularity and avascularity. Untreated cartilage defects display an increased propensity to degenerate, leading to osteoarthritis (OA). During OA progression, articular chondrocytes are subjected to significant alterations in gene expression and phenotype, including a shift towards a hypertrophic-like state (with the expression of collagen type X, matrix metalloproteinases-13, and alkaline phosphatase) analogous to what eventuates during endochondral ossification. Present OA management strategies focus, however, exclusively on cartilage inflammation and degradation. A better understanding of the hypertrophic chondrocyte phenotype in OA might give new insights into its pathogenesis, suggesting potential disease-modifying therapeutic approaches. Recent developments in the field of cellular/molecular biology and tissue engineering proceeded in the direction of contrasting the onset of this hypertrophic phenotype, but knowledge gaps in the cause-effect of these processes are still present. In this review we will highlight the possible advantages and drawbacks of using this approach as a therapeutic strategy while focusing on the experimental models necessary for a better understanding of the phenomenon. Specifically, we will discuss in brief the cellular signaling pathways associated with the onset of a hypertrophic phenotype in chondrocytes during the progression of OA and will analyze in depth the advantages and disadvantages of various models that have been used to mimic it. Afterwards, we will present the strategies developed and proposed to impede chondrocyte hypertrophy and cartilage matrix mineralization/calcification. Finally, we will examine the future perspectives of OA therapeutic strategies.

Indexed as

Cartilage, ArticularOsteoarthritisCell DifferentiationChondrocytesHumansHypertrophycartilagehypertrophyosteoarthritissignaling pathway

Identifiers

PMID36552796
PMCPMC9777397
OpenAlexW4311478770

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.