Level D· Scientific groundwork from lab and animal studiesNarrative ReviewPubMed

Zinc transporter ZIP13 in mesenchymal tissues: From intracellular metal distribution to systemic homeostasis.

Hara T., Yoshigai E., Nakayama Y., Fukada T.

Narrative Review on Cardiovascular Disease, published in J Oral Biosci (2026) — 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
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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
J Oral Biosci (2026)
Country
Netherlands
Reported sample size
—
Source database
PubMed
PMID
42361527
DOI
10.1016/j.job.2026.100798

Abstract (original English)

Zinc is an essential trace element that plays pivotal roles in development, immunity, inflammation, and aging. Precise regulation of intracellular zinc distribution is mediated by zinc transporters of the ZIP (SLC39) and ZnT (SLC30) families, and their functions are increasingly recognized as tissue- and organelle-specific. Among these transporters, ZIP13 (SLC39A13) is a key regulator of mesenchymal biology. Genetic studies have demonstrated that loss of ZIP13 function causes connective tissue abnormalities, impaired bone and tooth development, and spondylodysplastic Ehlers-Danlos syndrome Type 3 in humans. ZIP13 is predominantly localized to the Golgi apparatus, where it regulates metal homeostasis and modulates zinc-dependent signalling pathways, including transforming growth factor beta and bone morphogenic protein signalling. Recent studies have expanded the functional landscape of ZIP13 beyond connective tissues, demonstrating its involvement in adipose tissue biology, skeletal muscle maintenance, cardiac homeostasis, and stem cell differentiation. In addition, patient-derived induced pluripotent stem cell models have provided new insights into ZIP13-dependent mesenchymal differentiation and regenerative biology. Emerging evidence indicates that ZIP13 can transport not only zinc but also iron, suggesting that ZIP13 functions as a metal distributor that regulates intracellu

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
HumansHomeostasisCation Transport ProteinsZincAnimalsMesodermCell DifferentiationSignal TransductionMesenchymal Stem Cells

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