Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Exploring the Potential of Calebin-A in Targeting Obesity-Related Genes and Pathways

Mahmoudi A., Saeedi-Boroujeni A., Karav S., Kesharwani P., Sahebkar A.

Laboratory Study on Type 2 Diabetes, published in J Cell Mol Med (2026) — 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
Laboratory Study
Journal
J Cell Mol Med (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42286733
PMCID
PMC13263248
DOI
10.1111/jcmm.71244

Abstract (original English)

Obesity is a global health crisis affecting millions, associated with metabolic disorders such as type 2 diabetes and cardiovascular disease. Calebin-A, a bioactive compound derived from Curcuma species, has shown promise in managing obesity and its complications. This study utilized bioinformatics tools to explore the molecular mechanisms of Calebin-A in obesity. Transcriptomic data from obese and normal omental adipose tissue (GSE286454) were analysed, identifying 317 differentially expressed genes (DEGs). Functional enrichment analysis indicated a notable engagement of lysosomal activity, immune response, cell migration, axon guidance and apoptosis pathways. A STRING-based protein-protein interaction network revealed nine hub genes through a composite centrality score. Among these, CTSB, CTSZ, CTSA, GRN and TUBB exhibited upregulation and were prioritized for subsequent analysis. External validation (GSE59034; 16 obese vs. 16 controls) corroborated the consistent upregulation of CTSB, CTSZ, GRN and CTSA. Target prediction analysis identified 443 potential targets for Calebin-A, with pathway-level overlap suggesting a convergence on immune, lysosomal and cytoskeletal processes. Molecular docking studies indicated favourable binding affinities (-5.2 to -7.1 kcal/mol), with CTSZ demonstrating the most robust interaction. A 100 ns molecular dynamics simulation validated structur

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

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

How we grade evidence
HumansObesityGene Expression ProfilingComputational BiologySignal TransductionGene Expression RegulationGene Regulatory NetworksTranscriptomeProtein Interaction MapsMolecular Docking Simulation

Browse all related research

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

Related research