Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Fractalkine is a key player in skeletal muscle metabolism and pathophysiology.

Swalsingh G., Pani P., Sadayappan S., Bal NC.

Narrative Review on Type 2 Diabetes, published in FEBS J (2025) — summary generated from the PubMed abstract.

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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
FEBS J (2025)
Country
England
Reported sample size
—
Source database
PubMed
PMID
40995677
DOI
10.1111/febs.70267

Abstract (original English)

Fractalkine (CX3CL1) is increasingly recognised for its role in regulating the metabolism of various tissues, including skeletal muscle. The circulating level of CX3CL1 is influenced by multiple organs including the brain, adipose tissue and immune cells, with skeletal muscles emerging as a significant source. Growing evidence shows that CX3CL1 modulates muscle metabolism through autocrine and paracrine mechanisms as well as influencing properties (i.e. migration, secretion, cellular communication) of local immune cells. Within skeletal muscle, CX3CL1-signaling is involved in the regulation of fibre-type composition, mitochondrial remodeling, local inflammation, and regenerative capacity. These actions affect muscle plasticity and adaptability in both resting and active states. CX3CL1 also facilitates substrate uptake, particularly glucose and lipids, by interacting synergistically with insulin-signaling pathways, especially during metabolic stress or exercise. Furthermore, CX3CL1 contributes to the coordination of skeletal muscle function with other key metabolic organs such as adipose tissue, liver and brain. Notably, CX3CL1 appears to play a role in the pathogenesis of several chronic diseases, including type 2 diabetes (T2D), obesity, cardiovascular disease (CVD), insulin resistance (IR) and arthritis. These findings underscore the relevance of CX3CL1 in both health and dis

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
HumansChemokine CX3CL1Muscle, SkeletalAnimalsSignal TransductionInsulin ResistanceDiabetes Mellitus, Type 2ObesityCardiovascular DiseasesAdipose Tissue

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