Puigserver Lab

#Throwback PERSPECTIVE | Mark Mattson The cyclic metabolic switching theory of intermittent fasting dlvr.it/TSL9Y6

We are pleased to announce the 2026 recipients of the AACR Scientific Achievement Awards. We look forward to celebrating their impactful contributions to cancer research at the AACR Annual Meeting. brnw.ch/21x1uIG #AACR26

Online Now: Regulation of skeletal muscle mitochondrial fuel utilization during exercise dlvr.it/TRgvcG #trends #endocrinology #metabolism

This is insane. BIG BREAKTHROUGH: Scientists just developed a CRISPR gene switch that helps heart cells rebuild their own power plants. Researchers have created a CRISPR based system that activates the gene PPARGC1A, which produces the metabolic regulator PGC-1α, the master controller of mitochondrial biogenesis. Instead of editing DNA, the system uses CRISPR activation (CRISPRa) to turn the gene on, triggering cells to naturally produce more mitochondria, the structures that generate ATP and power cellular metabolism. When tested in human cardiomyocytes and donor heart tissue, the technique significantly increased mitochondrial respiration and oxygen consumption, clear indicators of stronger cellular energy production. This matters because heart failure is fundamentally an energy crisis. After a myocardial infarction, mitochondria become dysfunctional and heart cells cannot generate enough ATP. About 1/3 of heart attack patients eventually develop heart failure, and around 6.8 million people in the U.S. live with the disease. Previous attempts to boost mitochondria forced cells into metabolic overdrive 👀! This CRISPR approach works differently. It fine-tunes the cell’s internal regulatory network, allowing mitochondria to increase in a controlled way without damaging metabolism. This new study shows that gene activation CRISPR systems can reprogram cellular metabolism, not just edit DNA. If future trials succeed, this approach could help treat: > Heart failure after heart attacks > Mitochondrial disorders > Metabolic diseases > Possibly neurodegenerative conditions

Activation of IRF3 in cardiomyocytes impairs mitochondrial oxidative function through PGC-1α inhibition and drives heart failure nature.com/articles/s4146…

Skeletal muscle-specific PGC-1α-b overexpression prevents eccentric contraction-induced muscle injury through an utrophin-independent pathway in mice physoc.onlinelibrary.wiley.com/doi/10.14814/p…

Good Sunday mito-friends, don't miss this new selection of papers related to #MitochondrialMedicine presorted by @Bims_BiomedNews biomed.news/bims-mitmed/20… Targeting PGC-1α axis Rescues Aberrant Development from Thyroid Hormone Defect in Brain Organoids

Potential health benefits of cold-water immersion: the central role of PGC-1α (open access) doi.org/10.1113/JP2895…

Victoria Sánchez Perez and Adam S. Crystal chaired a plenary session on "Synthetic Lethality" this morning at #Targets25, featuring Edmond M. Chan, Peter S. Hammerman, Francisca Vazquez, and William Sellers. @DrFranVazquez

Chaperone-mediated autophagy stabilizes PGC1α, influencing energy metabolism. Lamp2a knockdown in mice BAT increases PGC1α, boosting metabolism. Insights into thermal stress! PMID:40360527, Nat Commun 2025, @NatureComms doi.org/10.1038/s41467… #AI #Pharma #BioMed #RNA #ASHG #ESHG

If you can only attend a handful of meetings next year, @CellSymposia #CSMito2026 should be a priority. It offers a comprehensive, top-to-bottom perspective on mitochondria, and brings together a diverse group of scientists from across the field. Visit: hubs.li/Q03NMhpN0

If you can only attend a handful of meetings next year, @CellSymposia #CSMito2026 should be a priority. It offers a comprehensive, top-to-bottom perspective on mitochondria, and brings together a diverse group of scientists from across the field. Visit: hubs.li/Q03NM3-S0

❤️Our October issue is out❤️Read about the RNA editing enzyme ADAR1 regulating atherosclerosis progression, PGC-1α and cardiac adaptation to exercise training, the role of LYVE1-macrophages in heart regeneration and peripheral artery disease, and more. nature.com/natcardiovascr…

7/9) Nuance note: The researchers also found that PGC1α, the master regulator of mitochondrial biogenesis, was a key player. Artificially boosting PGC1α in the fathers’ muscles was enough to replicate the benefits in the offspring, though the exact link between muscle PGC1α and sperm microRNAs is still being worked out. This adds another layer to this fascinating mechanism.

New! Online now: Paternal exercise confers endurance capacity to offspring through sperm microRNAs dlvr.it/TNWKHB

Check out the latest paper from the Spiegelman lab that we collaboratored on looking into the role of cardiac PGC1a in adaptations to exercise. Congrats to Sumeet and all the other co-authors!

Skeletal muscle endothelial dysfunction through the activin A–PGC1α axis drives progression of cancer cachexia nature.com/articles/s4301…

A great line-up of speakers for Cell Symposia Multifaceted Mitochondria June 2026 in Glasglow! Check it out and register early: cell-symposia.com/mitochondria-2… @KivancBirsoy @RutterLab @jourdainlab and more! #mitochondria @CellPressNews

A postnatal molecular switch drives activity-dependent maturation of parvalbumin interneurons: Cell cell.com/cell/fulltext/…

#CIBseminars Mechanisms of mitochondrial adaptive respiration Pedro Latorre Muro, Dana-Farber Cancer Institute/Harvard Medical School, Boston, MA (USA) 📆July 17 ⏰15pm Online seminar. Registration required 🔗rediris.zoom.us/meeting/regist…