Evidence map›Paper›PMID 35327669›Full record

ArticleBiomolecules2022

Effects of the Leptin-Mediated MAPK/ERK Signaling Pathway on Collagen II Expression in Knee Cartilage of Newborn Male Mice from Obese Maternal Offspring.

Wenji Wang, Jialing Zhang, Yu Huo, Yuanzheng Zheng, Yonghao Gui

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2022. 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
4.6field-weighted citation impact, top 5% 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, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Maternal high-fat high-sugar diet impairs bone quality and strength but not cartilage in aging mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Adipokine Signaling Pathways in Osteoarthritis.Frontiers in bioengineering and biotechnology · 2022
    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

5 authors at 1 institution in 1 country.

Wenji WangNational Children's Medical Center, Children's Hospital, Fudan University, Shanghai 201102, China.ORCID 0000-0002-8215-1034
Jialing ZhangNational Children's Medical Center, Children's Hospital, Fudan University, Shanghai 201102, China.
Yu HuoNational Children's Medical Center, Children's Hospital, Fudan University, Shanghai 201102, China.
Yuanzheng ZhengNational Children's Medical Center, Children's Hospital, Fudan University, Shanghai 201102, China.
Yonghao GuiNational Children's Medical Center, Children's Hospital, Fudan University, Shanghai 201102, China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidemiological data suggest that various noncommunicable diseases develop as a result of altered maternal metabolic and physiological status due to exposure to several adverse factors during pregnancy. However, evidence for intrauterine exposure factors and mechanisms underlying the origin of early cartilage disease in chronic osteoarthritic disease is still lacking. In this study, we found that persistent overnutrition during pregnancy in obese mothers led to cartilage damage in neonatal male mice. This was mainly characterized by increased apoptosis with decreased expression of chondrocyte collagen II and low expression of Runx family transcription factor 2 (RUNX2) and SRY-box transcription factor 9 (SOX9). This reduction was also found to be associated with high leptin expression in newborn male mice of obese maternal offspring. Furthermore, the administration of leptin and mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase (ERK) inhibitors in primary chondrocytes showed that leptin mediated MAPK/ERK signaling activation and thus affected the key regulators of cartilage matrix metallopeptidase 1 (MMP1) and tissue inhibitor of metalloproteinase 1 (TIMP1), thereby altering the expression of collagen II in mouse cartilage. Altogether, this study provided insights into the molecular mechanisms of cartilage-related disease development and also new clues and evidence for the fetogenetic origin of cartilage diseases.

Indexed as

LeptinMitogen-Activated Protein KinasesAnimalsCartilageCells, CulturedCollagenMaleMiceObesitySignal TransductionTissue Inhibitor of Metalloproteinase-1CollagenLeptinMitogen-Activated Protein KinasesTissue Inhibitor of Metalloproteinase-1cartilagecollagen IIleptinMAPK/ERK signaling pathwayobese maternal offspring

Identifiers

PMID35327669
PMCPMC8946789
OpenAlexW4221092284

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.