Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Will reducing adopogenesis in bone increase bone mass?: PPARgamma2 as a key target in the treatment of age-related bone loss.

Duque G.

Narrative Review, published in Drug News Perspect (2003) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Drug News Perspect (2003)
Country
United States
Reported sample size
—
Source database
PubMed
PMID
12973444
DOI
10.1358/dnp.2003.16.6.829305

Abstract (original English)

There are several mechanisms that explain the pathophysiology of senile osteoporosis. One of them is the increasing levels of adipogenesis in bone marrow that are seen during the aging process. It is known that mesenchymal stem cells expressing a ligand-activated transcription factor known as peroxisome proliferator-activated receptor gamma(2) (PPARgamma(2)) are committed to differentiate into adipocytes. The regulation of PPARgamma(2) activation may play a role in the control of adipogenic differentiation of mesenchymal stem cells and thus contribute to their differentiation into osteoblasts in order to form new bone. In this review we describe the characteristics of the orphan receptor family of PPARs, with emphasis on PPARgamma(2), its structural and functional characteristics and its potential as a therapeutic target for the treatment of senile osteoporosis.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AdipocytesAgingBone Marrow CellsBone and BonesCell DifferentiationHumansOsteoporosisReceptors, Cytoplasmic and NuclearTranscription Factors

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.