As we age, we don’t recover from injury or illness like we did when we were young. But new research from UCSF has found gene regulators—proteins that turn genes on and off—that could restore the aging body’s ability to self-repair.
The scientists looked at fibroblasts, which build the scaffolding between cells that give shape and structure to our organs.
Fibroblasts maintain this scaffolding in the face of normal wear, disease, and injury. But over time, they slow down, and the body suffers.
JUST PUBLISHED: programmable macrophage mimics for inflammatory meniscus regeneration via nanotherapy
Click here to read the latest free, Open Access Article from Research.
The meniscus is a fibrocartilaginous tissue and organ in the human knee joint that serves critical functions, including load transmission, shock absorption, joint stability, and lubrication. Meniscal injuries are among the most common knee injuries, typically caused by acute trauma or age-related degeneration [1– 3]. Minor meniscal injuries are usually treated with in situ arthroscopic procedures or conservative methods, whereas larger or more severe injuries often necessitate total meniscus replacement. Recent advances in materials science and manufacturing techniques have enabled transformative tissue-engineering strategies for meniscal therapy [4, 5]. Several stem cell types, including synovium-derived mesenchymal stem cells, bone-marrow-derived mesenchymal stem cells, and adipose-derived stem cells (ADSCs), have been investigated as candidate seed cells for meniscal regeneration and repair. Notably, ADSCs are clinically promising because of their ease of harvest, high inducibility, innate anti-inflammatory properties, and potential to promote fibrocartilage regeneration [6– 8]. Our group has developed a series of decellularized matrix scaffolds for auricular, nasal, tracheal, and articular cartilage repair using 3-dimensional (3D) bioprinting techniques, successfully repairing meniscus defects and restoring physiological function [9– 12]. However, current tissue-engineering strategies for meniscus defect repair commonly rely on a favorable regenerative microenvironment. Pathological conditions such as osteoarthritis (OA) [13 – 16], the most prevalent joint disorder, often create inflammatory environments that severely hinder meniscus regeneration [17 – 21]. Moreover, meniscal injury exacerbates the local inflammatory milieu, further impeding tissue healing and inevitably accelerating OA progression. Therefore, there is an urgent need to establish a cartilaginous immune microenvironment that first mitigates early-stage inflammation after meniscal injury and then sequentially promotes later-stage fibrocartilage regeneration [22 – 25].
Currently, targeted regulation using small-molecule drug injections is commonly employed to treat inflammatory conditions in sports medicine [26,27]. Most of these drugs exhibit broad-spectrum anti-inflammatory effects and inevitably cause varying degrees of side effects by activating nonspecific signaling pathways. Polyethyleneimine is a highly cationic polymer. It is widely used to modulate inflammation by adsorbing and removing negatively charged proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6), via electrostatic interactions [28–31]. Notably, modifying polyethyleneimine into its branched form (branched polyethyleneimine [BPEI]) has been shown to improve cytocompatibility and enhance in vivo metabolic cycling.
A newly identified and rare genetic variant slows the growth of mutated blood stem cells, researchers report in Science, and it reduces the risk of leukemia.
The findings offer insight into why some people are naturally more resistant to clonal expansion and age-related blood cancers despite acquiring risky mutations.
Learn more in a new Science Perspective.
A genome-wide association study identifies a genetic variant that reduces the risk of leukemia.
Francisco Caiado and Markus G. Manz Authors Info & Affiliations
Science
Wrap up for 2025.
Every year I compile what I think were some important contributions to longevity research. Here is my list for 2025!!
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through PayPal — https://paypal.me/sheekeyscience?coun… through Patreon — / thesheekeyscienceshow TIMESTAMPS: 00:00 – Intro & “What is aging?” / Hallmarks 2025 02:07 – Cellular reprogramming 05:47 – Senescent cells 11:45 – GLP‑1 agonists & ITP 13:43 – Elastin fragments & ECM aging 15:22 – Cardiac ‘age‑switch’ experiment 16:18 – Systemic environment: FOXO3 cells, antler EVs, plasma exchange 19:26 – Things you wouldn’t have thought of: AI-predicted antibodies REFERENCES: What is aging / hallmarks Hallmarks of aging update 2025 (14 hallmarks, ECM + psychosocial isolation) https://www.sciencedirect.com/science… reprogramming Prevalent mesenchymal drift in aging and disease is reversed by partial reprogramming – Cell 2025 https://doi.org/10.1016/j.cell.2025.0… A single factor for safer cellular rejuvenation (SB000) – bioRxiv 2025 https://doi.org/10.1101/2025.06.05.65… https://www.biorxiv.org/content/10.11… OpenAI x Retro Biosciences: AI‑designed reprogramming factors https://openai.com/index/accelerating… Restoration of neuronal progenitors by partial reprogramming in the aged neurogenic niche – Nature Aging 2024 (YouthBio’s scientific basis) https://doi.org/10.1038/s43587-024-00… Chemical reprogramming ameliorates cellular hallmarks of aging and extends lifespan in Caenorhabditis elegans – EMBO Molecular Medicine 2025 https://doi.org/10.1038/s44321-025-00… https://pmc.ncbi.nlm.nih.gov/articles… Senescent cells An unbiased cell‑culture selection yields DNA aptamers as senescence‑specific reagents – Aging Cell 2025 https://doi.org/10.1111/acel.70245 Senolytic CAR T cells reverse senescence‑associated pathologies – Amor et al., Nature 2020 https://doi.org/10.1038/s41586-020-24… Anti‑uPAR CAR T cells reverse and prevent aging‑associated defects in intestinal regeneration and fitness – Nature Aging 2025 https://doi.org/10.1038/s43587-025-01… Rejuvenation of Senescent Cells, In Vitro and In Vivo, by Low‑Frequency Ultrasound – Aging Cell 2025 https://pmc.ncbi.nlm.nih.gov/articles… Supplements, ITP & GLP‑1s Are GLP‑1s the first longevity drugs? – Nature Biotechnology 2025 https://doi.org/10.1038/s41587-025-02… GLP‑1 receptor agonists at the crossroads of metabolism and longevity – Nature Aging https://www.nature.com/articles/s4151… Extension of lifespan by epicatechin, halofuginone and mitoglitazone in male but not female UM‑HET3 mice – GeroScience 2025 https://doi.org/10.1007/s11357-025-01… https://pubmed.ncbi.nlm.nih.gov/40973… ECM, elastin & cardiac environment Elastin‑derived extracellular matrix fragments drive aging through innate immune activation – Nature Aging 2025 https://doi.org/10.1038/s43587-025-00… Sun, A.R., Ramli, M.F.H., Shen, X. et al. Hybrid hydrogel–extracellular matrix scaffolds identify biochemical and mechanical signatures of cardiac ageing. Nat. Mater. 24, 1489–1501 (2025). https://doi.org/10.1038/s41563-025-02… Systemic environment: stem cells, EVs, plasma Senescence‑resistant human mesenchymal progenitor cells counter aging in primates – Cell 2025 https://doi.org/10.1016/j.cell.2025.0… Attenuation of primate aging via systemic infusion of senescence‑resistant cells – https://pmc.ncbi.nlm.nih.gov/articles… Extracellular vesicles from antler blastema progenitor cells reverse bone loss and mitigate aging‑related phenotypes – Nature Aging 2025 https://pmc.ncbi.nlm.nih.gov/articles… Human clinical trial of plasmapheresis effects on biomarkers of aging – Aging Cell 2025 https://pmc.ncbi.nlm.nih.gov/articles… “Things you wouldn’t think of” – AI antibodies Atomically accurate de novo design of antibodies with atomic precision – Baker Lab, Nature 2025 https://doi.org/10.1038/s41586-025-09… Computational design of human antibodies targeting any antigen – https://doi.org/10.1016/j.cell.2025.1… Please 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:
Singapore has one of the highest life expectancies in the world, yet many individuals spend almost a decade in poor health toward the end of life. Scientists from the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine) are working to understand how aging itself can be modified to prevent age-related diseases, including Alzheimer’s disease.
A new study led by Professor Brian K Kennedy, Department of Biochemistry, Chair of the Healthy Longevity Translational Research Program (TRP), NUS Medicine, has discovered that calcium alpha-ketoglutarate (CaAKG), a safe, naturally occurring metabolite commonly studied for healthy aging, can restore key memory-related brain functions that have been disrupted in Alzheimer’s disease.
The paper is published in the journal Aging Cell.
A landmark 2024 study reveals the staggering danger of our sedentary lifestyles, with a 300% higher risk of mortality for those who barely move. But there’s a simple, powerful antidote already within your reach. In this update, we dive into the data showing how just 15 minutes of daily walking can dramatically slash your risk and add healthy years to your life, ensuring you’re here to benefit from the incredible age-reversal breakthroughs on the horizon.
The future is arriving faster than you think. We’re also bringing you an exclusive, first-look update on the revolutionary OSK (Yamanaka factor) research aimed at reversing biological aging. From groundbreaking success in mice to imminent primate trials, we break down the timeline and science that could make meaningful age reversal a human reality. Don’t let a sedentary present cut short your chance at a longer, younger future.
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How do we slow down atherosclerosis? Researcher Amanda Foks believes this is possible by eliminating aging immune cells. This would represent a completely new treatment for heart attacks and strokes. For this research, she has received the Established Investigator Dekker Grant from the Dutch Heart Foundation.
Hoe remmen we slagaderverkalking af? Onderzoeker Amanda Foks denkt dat dit mogelijk is door verouderde afweercellen uit te schakelen. Dat zou een geheel nieuwe behandeling tegen hart-en herseninfarcten zijn. Voor dit onderzoek ontvangt ze de Established Investigator Dekkerbeurs van de Hartstichting.
Slagaderverkalking ontstaat doordat vetten en cellen zich jarenlang ophopen in de vaatwand. Vaak merk je daar niets van, totdat zo’n verdikking plotseling scheurt. Dan kan er acuut een hart-of herseninfarct ontstaan.
Met de leeftijd neemt het risico toe: bloedvaten worden minder soepel en het afweersysteem werkt minder goed, waardoor ontstekingen ontstaan. Die ontstekingen versnellen juist weer de slagaderverkalking.
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Shan, W., Liu, Y., Tang, R. et al. Targeting mitochondrial autophagy for anti-aging. Cell Death Discov. (2025). https://doi.org/10.1038/s41420-025-02913-y.