He makes sure to tell people he did not make embryos.
Friends, I did NOT create a human clone. What I did create are induced pluripotent stem cells (iPSCs) — cells that can potentially become many different cell types and may one day help repair the body.
It’s one of the most promising technologies in regenerative medicine, and is already being explored in clinical research.
The science is fascinating, the ethical questions are important, and both deserve thoughtful discussion.
The Central Social Insurance Medical Council, which advises the health minister, on Wednesday approved the application of public health insurance to RiHeart, a cardiac muscle cell sheet that uses induced pluripotent stem (iPS) cells, effective on Sept. 1.
It is the second case of insurance coverage approval in the country for an iPS cell-derived regenerative medicine product.
Created by introducing specific genes into the cells of blood and skin, iPS cells are versatile in that they possess the ability to grow into the cells of various tissues and organs.
Can an engineered enzyme repair molecular damage that was once thought permanent? Dr. Aubrey de Grey explains why CMLase may be an important proof of concept for longevity research—and what still has to be proven.
In this episode, Tim Ventura speaks with Dr. Aubrey de Grey, founder, President and Chief Science Officer of the Longevity Escape Velocity Foundation, about a striking new result from researchers at Revel Pharmaceuticals.
The researchers developed an enzyme called CMLase to target Nε-carboxymethyl-lysine, or CML is an advanced glycation end product that accumulates on long-lived proteins in tissues including the skin, arteries and lens of the eye. It has historically been considered a stable and effectively irreversible form of molecular damage.
After screening and evolving more than 500 million enzyme variants, the team created CMLase, which oxidizes CML and restores the affected amino acid to its native lysine form.
In laboratory experiments involving donated human tissue, CMLase reduced CML burden by more than 70% in aged arterial sections and more than 55% in aged skin sections. In the skin samples, post-treatment CML staining was lower than that observed in tissue from a 31-year-old donor. The researchers also demonstrated reductions in CML in human lens proteins.
This does not mean that a person has had their aging reversed.
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This is rather technical.
Researchers at Revel Pharmaceuticals and Calico Life Sciences have engineered CMLase, an enzyme that removes carboxymethyl-lysine (CML) — a glycation product long considered permanent damage on our longest-lived proteins. In this video I explain the details behind this discovery and what it means for the aging field.
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through PayPal — https://paypal.me/sheekeyscience?coun… through Patreon — / thesheekeyscienceshow TIMESTAMPS 0:00 – Intro: what CML is and why it seemed irreversible 2:25 – How they made the enzyme 6:20 – Human tissue data 7:40 – My thoughts and limitations Paper: Trabosh et al., Nature Communications, 2026 — https://doi.org/10.1038/s41467-026-75… note that The Sheekey Science Show is distinct from Eleanor Sheekey’s teaching and research roles. The information provided in this show is not medical advice, nor should it be taken or applied as a replacement for medical advice. The Sheekey Science Show and guests assume no liability for the application of the information discussed. Icons in intro; “https://www.freepik.com/free-photos-v…“Background vector created by freepik — www.freepik.com.
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TIMESTAMPS
Current barriers to achieving radical life extension include the inability to use syngeneic, youthful mesenchymal stem cells (MSCs) and the anti-regenerative effects of senescence-associated secretory phenotype (SASP) factors. We aim to overcome this by a combination approach in which senescent cell burden is reduced utilizing SenoVax™ a dendritic cell based senolytic immunotherapy combined with syngeneic pluripotent stem cell derived MSC.
We induced hepatic injury and accelerated aging using two established murine models: carbon tetrachloride (CCl₄) mediated liver injury and doxorubicin induced systemic senescence. Animals were treated with control, SenoVax, pMSCs or the combination. Outcomes included biochemical and histologic indices of liver injury, circulating and tissue biomarkers of senescence (IL-11, YKL-40, IL-6, IL-23 R) and regeneration (Klotho, FGF-2, neo-VEGF, GDF-11).
Both CCl₄ and doxorubicin induced a robust senescent phenotype characterized by increased pro-inflammatory and pro-fibrotic mediators and downregulation of regenerative biomarkers. Combined senolytic and pMSC therapy outperformed mono therapies and produced clear synergistic benefits, including significant biochemical improvement of liver failure parameters, reversal of accelerated aging features, and restoration of regenerative signaling pathways. Senolytic monotherapy yielded partial improvements, while pMSCs alone showed limited activity in the presence of a high senescent-cell burden.
Fifteen years ago, I sat down with the father of virtual reality, and he told me the Singularity was a religion for geeks.
I disagreed with him. To his face.
Jaron Lanier was no technophobe. He built the tech. He just refused to worship it. In 2011, that made him an outlier. Everyone in my orbit was mapping exponential curves and setting dates for digital immortality.
Now look at the culture around #AI.
We have prophets and prophecies, heretics and true believers, people who genuinely expect a machine god to arrive and solve death, meaning, and the economy on our behalf. Lanier saw the shape of that faith before most of us would admit it was a faith at all.
I still think he was wrong about parts of it. I also think he was early on the part that matters most: technology is the How. It was never going to answer the Why or the What. That is the work a religion does, and for a lot of brilliant people the #Singularity quietly became exactly that.