Over the past few years, excitement around MUSE cells has grown quickly, fueled in part by media coverage of Dr. Adeel Khan, a physician known for adopting new and experimental therapies early and who has gained a degree of infamy in certain academic circles for doing so. A now-removed USA Today article previously highlighted his efforts to bring MUSE cell therapy to the United States, drawing significant public attention. That kind of exposure naturally generates interest, but it also underscores the need to separate early promise from established evidence.

I had the opportunity to speak alongside Dr. Khan at the TOBI conference in 2019. He is often on the leading edge of medical innovation, but he is also often an early adopter before adequate human research has been published. That is not necessarily wrong, but it does make clear communication essential. Patients deserve to know the difference between early promise and proven treatment.

MUSE cells are a great example. The biology is genuinely fascinating. The early data in some medical fields are encouraging. But when it comes to orthopedics, the gap between the excitement and the evidence is still wide. If you are hearing that MUSE cells are already a proven treatment for joints, tendons, cartilage, or anti-aging, that claim is ahead of the science.

What Are MUSE Cells?

MUSE stands for multilineage differentiating stress-enduring cells. They are a rare naturally occurring subpopulation found within mesenchymal stromal cell populations and in connective tissues throughout the body. Depending on the source and study, they make up roughly 1 to 3 percent, and sometimes up to 5 percent, of the broader mesenchymal cell population [1-3,12,13].

What makes them so interesting is that they appear to combine two features that usually do not coexist easily in regenerative medicine: pluripotent like behavior and a relatively favorable safety profile. MUSE cells express pluripotency related markers such as Nanog, Oct3/4, and Sox2, and they can differentiate into cell types from all three germ layers. At the same time, unlike embryonic stem cells or induced pluripotent stem cells, they have shown low tumorigenic risk, low telomerase activity, and no teratoma formation in the settings studied so far [1-4,12,13].

Another major point of interest is their ability to home to sites of tissue injury. They appear to follow the S1P S1PR2 signaling axis, meaning damaged tissues release a signal and MUSE cells can migrate toward it after intravenous administration [5,12,19]. That is part of what has made them so attractive for conditions where targeted delivery is otherwise difficult.

MUSE cells also appear to have a degree of immune privilege. They express HLA G, which may allow allogeneic use without HLA matching or long term immunosuppression [1,19]. If that continues to hold up in larger studies, it would be a meaningful advantage.

Why MUSE Cells Have Generated So Much Interest

The field has focused on MUSE cells because they potentially address several limitations that have dogged other cell based therapies. In theory, they may be able to:

  • travel to areas of injury after intravenous infusion
  • survive in stressed environments
  • differentiate into tissue compatible cells
  • avoid uncontrolled growth
  • function in allogeneic settings without long term immune suppression

That is a compelling list. It is also still largely a research story, especially in orthopedics.

Orthopedic Applications: Promising Preclinical Work, But No Human Trials

This is the key point for musculoskeletal medicine.

As of now, there are no published human clinical trials of MUSE cells for orthopedic conditions. Not for knee osteoarthritis. Not for tendon disease. Not for ligament injuries. Not for bone healing. Not for cartilage restoration in humans [20].

The orthopedic evidence people most often point to comes from a rat osteochondral defect model. In that study, human bone marrow derived MUSE cells were transplanted into immunodeficient rats with cartilage and bone defects in the patellar groove. At 12 weeks, the MUSE treated group showed a smoother, more hyaline like cartilage surface and better subchondral bone restoration compared with both controls and non MUSE cell groups [20].

That is encouraging, and it suggests MUSE cells may support both chondrogenic and osteogenic repair in a controlled preclinical setting. It also supports the idea that MUSE cells may represent a more biologically active subpopulation than conventional heterogeneous MSC preparations [12,20].

But we have to be disciplined about what this does and does not mean.

It does not mean MUSE cells have been proven to help human knee arthritis.
It does not mean they are ready for routine orthopedic use.
It does not mean they outperform well studied autologous orthobiologics in actual musculoskeletal patients.

There is still a major translational gap. We do not yet have:

  • large animal orthopedic studies
  • human orthopedic safety trials
  • human orthopedic efficacy trials
  • long term orthopedic durability data

That is a lot of missing information.

Why the Orthopedic Gap Matters

It is easy to assume that if a therapy looks promising in neurology or cardiology, it should also work for joints, tendons, and cartilage. That is not how biology works.

Musculoskeletal tissues are mechanically unique. Cartilage, tendon, ligament, and bone exist in high load environments and have very different healing demands than brain or heart tissue. Even if MUSE cells can survive and differentiate in one tissue type, that does not guarantee they will behave the same way in another.

Right now, the orthopedic case for MUSE cells is built mainly on:

  • preclinical plausibility
  • one rat osteochondral repair study
  • broader regenerative biology arguments

That is not enough to justify confident clinical claims.

Where the Human Data Are Stronger: Neurology

If there is one area where MUSE cells have moved past pure theory, it is neurology.

Stroke

This is the strongest human clinical signal so far. In a randomized placebo controlled trial of CL2020, an allogeneic MUSE cell product, patients with subacute ischemic stroke were treated 14 to 28 days after stroke. The response rate, defined by meaningful functional improvement, was 40 percent in the treatment group versus 10 percent in placebo [8].

Preclinical stroke studies also showed that MUSE cells could survive, differentiate into neuronal lineage cells, integrate into neural circuits, and support functional recovery [6,15,16,20].

That is a real signal. It still needs replication in larger trials, but it is much more substantial than anything that currently exists in orthopedics.

Spinal Cord Injury

Early work in spinal cord injury is also promising. In a human clinical trial involving cervical traumatic spinal cord injury, intravenous administration of a single dose of allogeneic MUSE cells was feasible, with no major safety concerns reported and statistically significant improvements from baseline in motor function, activities of daily living, and quality of life [9].

Amyotrophic Lateral Sclerosis

In ALS, repeated monthly infusions were generally well tolerated. Some patients showed slower functional decline, but the study was small and the results remain preliminary [11].

Neonatal and Other Neurologic Conditions

There are also translational and animal studies in perinatal hypoxic ischemic brain injury and other neurologic settings [15-17].

So yes, there is real reason for scientific interest in MUSE cells. It is just important not to pretend that neurologic promise automatically equals orthopedic proof.

Other Medical Applications

Beyond neurology, MUSE cells have shown interesting signals in other disease categories.

Cardiac Disease

In animal models of myocardial infarction, MUSE cells have shown the ability to home to damaged myocardium, reduce infarct size, improve ventricular function, and support long lasting tissue repair [5]. A first in human study in acute myocardial infarction also suggested feasibility and early safety, but the sample size was very small [10].

Liver, Kidney, and Skin Applications

Preclinical work has also suggested possible roles in hepatic fibrosis, nephropathy, wound repair, epidermolysis bullosa, and other tissue injury states [2,18,21].

These data reinforce that MUSE cells may eventually have broad medical applications. They do not solve the orthopedic evidence gap.

Safety: Encouraging, But Still Incomplete

One of the strongest arguments in favor of MUSE cells is the safety profile seen so far.

Across animal studies and early human trials:

  • tumor formation has not been observed
  • allogeneic administration has been possible without routine immunosuppression
  • immune rejection has not been a major signal in the data currently available [1,2,8,9,19]

That is all encouraging.

But “encouraging” is not the same as “fully established.” There was at least one grade 4 status epilepticus event in the stroke trial, although causality is difficult to interpret in stroke patients [8]. More importantly, long term human follow up remains limited. For a living cell based therapy that may survive and function in tissue for prolonged periods, that matters.

Anti Aging and Healthspan: Interesting Theory, Not Clinical Proof

There is increasing discussion about whether MUSE cells could eventually have a role in healthspan optimization or anti aging. The theoretical logic is understandable. If these cells can replace damaged cells, reduce inflammation, and support tissue integrity, maybe they could also help preserve function with aging [14,22,24].

But at this point, that remains speculative.

There are no robust clinical trials showing that MUSE cells improve longevity or healthspan in humans. Reviews discussing this possibility are interesting and worth reading, but they are not proof [22,24,25].

Any clinic claiming MUSE cells are already an anti aging treatment is making a claim that goes beyond the evidence.

Media Hype, Celebrity Influence, and Medical Tourism

This is where the conversation gets more complicated.

A November 2025 article from The Niche raised concerns about celebrity promotion of MUSE cells after Kim and Khloé Kardashian reportedly received these treatments in Mexico from Dr. Adeel Khan. The article’s central argument was not that MUSE cells are impossible or inherently fraudulent, but that the current public messaging is moving far faster than the data, especially when celebrities help normalize treatments that remain experimental [26].

The concerns raised in that article are worth taking seriously:

  • MUSE cells have relatively narrow published clinical data compared with how broadly they are being promoted [26].
  • Many of the strongest claims involve chronic pain, injury recovery, and longevity, even though published human data remain sparse or absent for those uses [26].
  • There are still scientific debates about what MUSE cells truly are, how reliably they can be isolated, and whether some markers used to define them are specific enough [3,4,7,26].
  • Clinics operating outside the United States may market these therapies for a wide range of conditions without publishing peer reviewed outcomes for those indications [26].

I agree with the broader caution. If someone is traveling outside the country for MUSE cell therapy, they should understand that they may not actually know:

  • how the cells were sourced
  • how the product was manufactured
  • how the cells were characterized
  • whether the dose and purity are consistent
  • whether the treatment being marketed matches anything that has been studied in a legitimate trial

That lack of transparency matters. Patients should not have to pay out of pocket to become the experiment.

Why Patients Should Be Skeptical of Unverified MUSE Cell Treatments

This is my practical concern.

The science is promising enough to create real excitement. That same promise also creates a perfect environment for clinics to get ahead of the evidence.

Here are the red flags I would watch for:

  • Clinics offering MUSE cells for orthopedic conditions without published human trials
  • Claims that MUSE cells are already proven for cartilage, tendon, ligament, or anti aging applications
  • Marketing that leans heavily on mechanisms and animal data while skipping over the lack of human orthopedic evidence
  • No transparency about sourcing, expansion, quality control, or characterization
  • No honest discussion of the fact that long term human safety remains incomplete
  • Broad cure all or longevity claims

The central problem is simple. A clinic may say it is offering MUSE cell therapy, but unless that product is manufactured and studied in a way that mirrors the published research, you do not actually know that you are receiving anything equivalent to what has been tested.

What the Field Still Needs

Before MUSE cells can reasonably move into mainstream orthopedic care, the field needs:

  • published human orthopedic trials
  • larger randomized controlled trials
  • long term safety follow up
  • large animal musculoskeletal studies
  • standardized manufacturing and characterization
  • clearer dose and route comparisons
  • better understanding of which patients are most likely to benefit
  • honest head to head comparisons against existing orthopedic options

Without that, the field remains promising but premature.

My Perspective

I am not dismissing MUSE cells. Far from it.

The biology is compelling. The early neurologic data are impressive. The apparent combination of injury homing, immune privilege, low tumorigenicity, and broad differentiation potential makes MUSE cells one of the more interesting regenerative platforms being studied right now.

But patients deserve discipline, not hype.

As of now, there are no published human orthopedic trials. That matters. If someone is offering MUSE cells for joints, tendons, ligaments, or anti aging, they are operating in a space where marketing is currently much stronger than orthopedic evidence.

At The Patel Center for Functional Regeneration, we continue to follow this research closely. Until peer reviewed human orthopedic data are available, my focus remains on evidence based autologous orthobiologics and other treatments with a stronger clinical foundation in musculoskeletal medicine.

The Bottom Line

MUSE cells may eventually become an important tool in regenerative medicine. The early work in stroke, spinal cord injury, and other fields suggests this is not just hype. There is real scientific promise here.

But in orthopedics, that promise has not yet matured into human clinical evidence.

For now, the right posture is cautious optimism. Watch the data. Demand transparency. Be skeptical of treatments being sold far ahead of the science.

If you are interested in learning more about the latest regenerative medicine research or exploring evidence based options for orthopedic pain and recovery, contact Dr. Shounuck Patel in Newport Beach, California to schedule a consultation.

References

  1. Kuroda Y, Oguma Y, Hall K, Dezawa M. Endogenous Reparative Pluripotent Muse Cells With a Unique Immune Privilege System: Hint at a New Strategy for Controlling Acute and Chronic Inflammation. Frontiers in Pharmacology. 2022;13:1027961. doi:10.3389/fphar.2022.1027961.

  2. Fisch SC, Gimeno ML, Phan JD, et al. Pluripotent Nontumorigenic Multilineage Differentiating Stress Enduring Cells (Muse Cells): A Seven-Year Retrospective. Stem Cell Research & Therapy. 2017;8(1):227. doi:10.1186/s13287-017-0674-3.

  3. Kuroda Y, Kitada M, Wakao S, et al. Unique Multipotent Cells in Adult Human Mesenchymal Cell Populations. Proceedings of the National Academy of Sciences of the United States of America. 2010;107(19):8639-43. doi:10.1073/pnas.0911647107.

  4. Li G, Wakao S, Kitada M, Dezawa M. Tumor Suppressor Let-7 Acts as a Key Regulator for Pluripotency Gene Expression in Muse Cells. Cellular and Molecular Life Sciences. 2024;81(1):54. doi:10.1007/s00018-023-05089-9.

  5. 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. doi:10.1161/CIRCRESAHA.117.311648.

  6. Park YJ, Niizuma K, Mokin M, Dezawa M, Borlongan CV. Cell-Based Therapy for Stroke: Musing With Muse Cells. Stroke. 2020;51(9):2854-2862. doi:10.1161/STROKEAHA.120.030618.

  7. Rajabi A, Akbarzadeh S, Tayefeh-Gholami S, Bonyadi M. The Promising Role of Muse Cells in Regenerative Medicine: Mechanisms, Applications, and Future Directions. Life Sciences. 2025;124024. doi:10.1016/j.lfs.2025.124024.

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  9. Koda M, Imagama S, Nakashima H, et al. Safety and Feasibility of Intravenous Administration of a Single Dose of Allogenic-Muse Cells to Treat Human Cervical Traumatic Spinal Cord Injury: A Clinical Trial. Stem Cell Research & Therapy. 2024;15(1):259. doi:10.1186/s13287-024-03842-w.

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  12. Kushida Y, Wakao S, Dezawa M. Muse Cells Are Endogenous Reparative Stem Cells. Advances in Experimental Medicine and Biology. 2018;1103:43-68. doi:10.1007/978-4-431-56847-6_3.

  13. Dezawa M. Muse Cells Provide the Pluripotency of Mesenchymal Stem Cells: Direct Contribution of Muse Cells to Tissue Regeneration. Cell Transplantation. 2016;25(5):849-61. doi:10.3727/096368916X690881.

  14. Dezawa M. Macrophage- And Pluripotent-Like Reparative Muse Cells Are Unique Endogenous Stem Cells Distinct From Other Somatic Stem Cells. Frontiers in Bioengineering and Biotechnology. 2025;13:1553382. doi:10.3389/fbioe.2025.1553382.

  15. Yamashita T, Kushida Y, Abe K, Dezawa M. Non-Tumorigenic Pluripotent Reparative Muse Cells Provide a New Therapeutic Approach for Neurologic Diseases. Cells. 2021;10(4):961. doi:10.3390/cells10040961.

  16. Suzuki T, Sato Y, Kushida Y, et al. Intravenously Delivered Multilineage-Differentiating Stress-Enduring Cells Dampen Excessive Glutamate Metabolism and Microglial Activation in Experimental Perinatal Hypoxic-Ischemic Encephalopathy. Journal of Cerebral Blood Flow and Metabolism. 2021;41(7):1707-1720. doi:10.1177/0271678X20972656.

  17. Ueda K, Sato Y, Shimizu S, et al. Systemic Administration of Clinical-Grade Multilineage-Differentiating Stress-Enduring Cells Ameliorates Hypoxic-Ischemic Brain Injury in Neonatal Rats. Scientific Reports. 2023;13(1):14958. doi:10.1038/s41598-023-41026-3.

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  25. Bhartiya D. Relationship Between VSELs, Muse Cells and MSCs in Health and Disease. Stem Cell Reviews and Reports. 2026. doi:10.1007/s12015-026-11078-9.

  26. Knoepfler P. Khloé & Kim Kardashian stem cell adventures in Mexico, MUSE cells raise concerns. The Niche. November 19, 2025.