The pinnacle of naturally occurring regenerative potential.

What makes them different ↓

Discovered 2010 — Tohoku University

A rare, naturally pluripotent cell.

Muse cells are a sparse subpopulation of mesenchymal stem cells, roughly one to three percent of an MSC pool. They carry the pluripotency marker SSEA-3, survive conditions that kill ordinary cells, and migrate to sites of physical distress on their own.

Mu Multilineage-differentiating
se Stress-enduring

In plain terms: cells that survive when nothing else does, and rebuild what they find broken into the tissue it was meant to be.

How Muse cells compare.

The standard alternatives in regenerative medicine, set against the properties patients and clinicians actually weigh.

Property MuseWhat we use Umbilical cordUC-MSC EmbryonichESC InducediPSC
Source Adult mesenchymal tissue Umbilical cord (Wharton's jelly) Donated embryos Reprogrammed somatic cells
Pluripotency All three germ layers Mesoderm only All three germ layers All three germ layers
Tumorigenic risk Minimal — none reported in human trials None reported Documented teratoma formation Documented teratoma formation
Injury-site homing Yes — S1P-guided Limited No No
Abundance 1–3% of MSC pool Abundant Limited Engineerable
Regulatory status Investigational (MX / Japan) COFEPRIS-regulated (MX) FDA-restricted FDA-restricted

Properties summarised from peer-reviewed sources. View references →

Muse cells, by the numbers.

Four anchor facts, each tied to its primary source.

1–3%

of the standard MSC pool is Muse-positive.

Kuroda Y, et al. Unique multipotent cells in adult human mesenchymal cell populations. PNAS 2010.

2010

First isolated at Tohoku University by the Dezawa lab.

Dezawa M, et al. Multilineage-differentiating stress-enduring (Muse) cells. Original report →

SSEA-3+

Surface marker used to identify and sort Muse cells from MSC pools.

Wakao S, et al. Multilineage-differentiating stress-enduring (Muse) cells. PNAS 2011.

0

Tumors reported across published Muse-cell human trials to date.

Multiple Phase I/II trials, 2018–2024. Trial summary →

How Muse cells reach injury.

The S1P-guided homing mechanism, traced from infusion to integration.

Nothing steers the cells to the damage. The injured tissue emits the signal itself, and the cells that can read it arrive on their own.

Mechanism references →
Muse cells enter the bloodstream by infusion, follow the sphingosine-1-phosphate gradient released by damaged tissue, and concentrate at the injury site. 02S1P gradient 03Injury site 01Infusion Bloodstream
  • Muse cell
  • Resident tissue
  • S1P gradient

Schematic — not to scale.

  1. 01

    Infusion

    Muse cells enter circulation by IV. No targeted delivery is required: the bloodstream is the delivery route.

    Wakao S, et al. PNAS 2011.
  2. 02

    S1P gradient detection

    Damaged tissue releases sphingosine-1-phosphate (S1P). Muse cells express the S1P receptor and follow the gradient toward its highest concentration.

    Yamada Y, et al. Biochem Biophys Res Commun, 2018.
  3. 03

    Migration + integration

    Muse cells concentrate at the injury site, differentiate into the resident tissue type (cartilage, neuron, hepatocyte), and integrate without forming teratomas.

    Kuroda Y, et al. PNAS 2010 (mechanism); Phase I/II trials 2018–2024 (safety).

Repair that meets the tissue where it is.

Standard mesenchymal cells modulate inflammation and signal repair, but rely on the body to do the building. Muse cells contribute that signaling and integrate directly into the damaged structure, behaving like the tissue they replace.

  1. 01

    Direct integration, not just signaling.

    Standard UC-MSCs orchestrate repair through paracrine signaling and fade. Muse cells differentiate into the resident cell type at the injury site and remain as functional tissue.

  2. 02

    Tissue-specific adaptation.

    Cartilage in a joint. Neurons in a stroke lesion. Hepatocytes in a damaged liver. Muse cells adopt the cell type appropriate to where they arrive, not a fixed lineage.

  3. 03

    Stress-tolerant survival.

    Originally isolated by what survived under severe cellular stress. That resilience translates to clinical use: more cells reach the injury alive, more integrate, fewer are lost in transit.

View Muse cell protocols →

References & further reading

The claims on this page rest on the peer-reviewed Muse-cell literature summarized below. These citations support the general scientific basis for Muse-cell biology; they are not claims of guaranteed outcomes for any individual patient. Muse-cell therapy is investigational: clinical evidence is still developing, and protocols at TrueCell are provided under Mexican regulatory authority (COFEPRIS) after individual physician review.

  1. Kuroda Y, Kitada M, Wakao S, et al. Unique multipotent cells in adult human mesenchymal cell populations. Proceedings of the National Academy of Sciences USA. 2010;107(19):8639–8643. PubMed
  2. Wakao S, Kitada M, Kuroda Y, et al. Multilineage-differentiating stress-enduring (Muse) cells are a primary source of induced pluripotent stem cells in human fibroblasts. Proceedings of the National Academy of Sciences USA. 2011;108(24):9875–9880. PubMed
  3. Dezawa M. Muse Cells Provide the Pluripotency of Mesenchymal Stem Cells: Direct Contribution of Muse Cells to Tissue Regeneration. Cell Transplantation. 2016;25(5):849–861. PubMed
  4. Yamada Y, Wakao S, Kushida Y, et al. S1P–S1PR2 Axis Mediates Homing of Muse Cells Into Damaged Heart for Long-Lasting Tissue Repair and Functional Recovery After Acute Myocardial Infarction. Circulation Research. 2018;122(8):1069–1083. PubMed
  5. Kuroda Y, Oguma Y, Hall K, et al. Endogenous reparative pluripotent Muse cells with a unique immune privilege system: Immunomodulatory properties and clinical application. Frontiers in Cell and Developmental Biology. 2022;10:1027961. PubMed

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