Evidence map›Paper›PMID 20683677›Full record

ArticleCellular & molecular biology letters2010

Leptin regulates MMP-2, TIMP-1 and collagen synthesis via p38 MAPK in HL-1 murine cardiomyocytes.

Kristin Schram, Sabrina De Girolamo, Siham Madani, Diana Munoz, Farah Thong, Gary Sweeney

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular biology letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. β-Nicotinamide mononucleotide blocks UVB-induced collagen reduction via regulation of ROS/MAPK/AP-1 and stimulation of mitochondrial proline biosynthesis.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  4. Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Progesterone Inhibits Leptin-Induced Invasiveness of BeWo Cells.International journal of medical sciences · 2015
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 at 1 institution in 1 country.

Kristin SchramDepartment of Biology, York University, Toronto, Canada.
Sabrina De Girolamo
Siham Madani
Diana Munoz
Farah Thong
Gary Sweeney
York University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

A clear association between obesity and heart failure exists and a significant role for leptin, the product of the obese gene, has been suggested. One aspect of myocardial remodeling which characterizes heart failure is a disruption in the balance of extracellular matrix synthesis and degradation. Here we investigated the effects of leptin on matrix metalloproteinase (MMP) activity, tissue inhibitor of metalloproteinase (TIMP) expression, as well as collagen synthesis in HL-1 cardiac muscle cells. Gelatin zymographic analysis of MMP activity in conditioned media showed that leptin enhanced MMP-2 activity in a dose- and time-dependent manner. Leptin is known to stimulate phosphorylation of p38 MAPK in cardiac cells and utilization of the p38 MAPK inhibitor, SB203580, demonstrated that this kinase also plays a role in regulating several extracellular matrix components, such that inhibition of p38 MAPK signaling prevented the leptin-induced increase in MMP-2 activation. We also observed that leptin enhanced collagen synthesis determined by both proline incorporation and picrosirius red staining of conditioned media. Pro-collagen type-I and pro-collagen type-III expression, measured by real-time PCR and Western blotting were also increased by leptin, effects which were again attenuated by SB203580. In summary, these results demonstrate the potential for leptin to play a role in mediating myocardial ECM remodeling and that the p38 MAPK pathway plays an important role in mediating these effects.

Indexed as

AnimalsCells, CulturedCollagenCulture Media, ConditionedHumansLeptinMatrix Metalloproteinase 2MiceMyocytes, Cardiacp38 Mitogen-Activated Protein KinasesProtein PrecursorsTissue Inhibitor of Metalloproteinase-1Ventricular RemodelingCollagenCulture Media, ConditionedLeptinMatrix Metalloproteinase 2p38 Mitogen-Activated Protein KinasesProtein PrecursorsTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID20683677
PMCPMC6275652
OpenAlexW2041901277

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.