The Hornberger Lab

1/ Why do muscles atrophy with aging and disuse? Is it because each tiny little myofibril gets smaller… or is it because we lose myofibrils? In our new study, we addressed this in humans and mice. biorxiv.org/cgi/content/sh… Full breakdown of the findings in this thread 👇

Memoir of Dr. Seals.... reveals the path he took to success in physiology and medical science. Along the way he encountered a series of daunting obstacles: laboratory flooding; pest infestations; children from local teams running through research areas... This should be great!

@kadance01 @grok is this real

The Mountain lion went crazy over his bike 😱😱

Center for Metabolic Health (CMH) at the University of Utah is inviting applications for our Postdoctoral Rising Stars in Metabolism held on Sept 2, 2026. If you are a postdoc with an exciting METABOLISM story, apply using the QR code by April 24. Please RT with colleagues.

During the PhD, whenever felt that I couldn't write I did one push-up. At the end of the PhD:

TAK1 regulates skeletal muscle mass, hypertrophic signaling, and metabolic homeostasis in male and female mice biorxiv.org/content/10.648…

This week's muscle science roundup is stacked. One of the strongest weeks I've seen: aging, hypertrophy, metabolism, disease mechanisms, and more. Whether you're a researcher or just care about your muscles, this is worth 5 minutes. 👇 biomed.news/bims-moremu/20… #myotwitter

LAMA2-related muscular dystrophy is a rare genetic disease for which there is currently no treatment available. We are happy to share our recent publication in Molecular Therapy, where we describe a unique linker-mediated gene therapy approach . doi.org/10.1016/j.ymth…

This muscle cell gatekeeper has implications for a broad range of muscle-related conditions. Using murine and human models, Siwen Xue @siwen_xue Daniel C. Berry @dcberrylab & team @WeillCornell show block of the protein PDGFRbeta enhances myofiber repair and regeneration, whereas activation of it slows down recovery by limiting cell size and fusion: doi.org/10.1172/JCI188… The image shows muscle regeneration in mice treated with the PDGFRbeta inhibitor SU16f. #myotwitter

Our new study is now published in Advanced Science We show that skeletal muscle retains a molecular memory of disuse Young muscle shows transcriptional resilience Aged muscle shows exaggerated vulnerability advanced.onlinelibrary.wiley.com/doi/10.1002/ad… @nih_sognsvann @nih_physicperf

NIH is advancing a Unified Funding Strategy to ensure clearer, more consistent funding decisions across all Institutes and Centers – without using paylines. Hear from over a dozen Institute and Center (IC) Directors on how this strategy aligns with their IC funding practices in this NIH Funding blog post. ➡️ grants.nih.gov/news-events/ni…

The reproducibility crisis is not mysterious. It is a predictable consequence of the incentive structure that governs academic institutions. In corporate environments, criticism that could reflect negatively on the organization is strongly discouraged. Public communication is almost uniformly positive. Internal dissent is carefully managed. The logic is straightforward: employees are expected to protect the organization’s reputation, because reputation influences brand, market position, investor confidence, and ultimately revenue. Criticism public or private can carry significant cost for career advancement. Universities were historically organized around different principles - open dissent, protected speech, and adversarial critique as engines of truth-seeking. But as academic institutions have become increasingly corporatized, they have adopted many of the same norms that govern companies. The shift is visible in professional academic culture. On linkedin and science twitter, public academic discourse resembles corporate discourse - it is dominated by mutual affirmation, humble self-promotion, and reflexive praise. “Great work!” becomes the response, independent of actual quality. Open criticism is no longer treated as a scholarly obligation but is often viewed as uncollegial and risky. Anyone interested in protecting their career quickly learns to minimize or eliminate criticism altogether. In tightly networked fields, even a single adversarial interaction can carry outsized consequences. When criticism generates friction, and friction carries professional risk, rational actors adapt. Scientists learn that visible positivity or silence is safer than challenging flawed work. This dynamic extends well beyond social media. Letters of recommendation become uniformly glowing. Peer review grows cautious and conformity-driven. Grant panels avoid adversarial debate. Institutional evaluations maintain positive framing over scrutiny. At the same time, academic status has become tightly coupled to journal name and , funding volume, citation metrics, and, identity politics. Under such conditions, the value of a study is derived from the journal it appears and who authored it, rather than from its underlying quality. In this environment, all findings are not appropriately stress-tested. They are accommodated, amplified, or politely ignored. The reproducibility crisis is not merely a failure of statistical methods. It is the product of a cultural transformation in which academia adopted corporate logic while retaining the rhetoric of open inquiry. As that gap widens, public trust in scientific institutions erodes accordingly.

We wrote this letter to address the overly rigid preregistration requirements imposed now by many journals on exploratory experimental physiology research - time to align guidelines with contemporary research methods! @proferikrichter @ISMCopenhagen physoc.onlinelibrary.wiley.com/doi/10.1113/EP…

IT ALL COMES DOWN TO SUNDAY. TEAM USA IS GOLD MEDAL GAME BOUND 🇺🇸🦅 #WinterOlympics

@RobWust Take a look at the details in the manuscript and then let me know if you think a collaboration is still viable with the samples you have. Feel free to email me.

@RobWust One of the keys for us to address this topic in a robust manner was the use of FIM-ID which permits automated myofibril level analyses. In our experience EM images are non conducive for such measurements. Samples need to be fixed and cryoprotected in a specific manner for FIM-ID

1/ Why do muscles atrophy with aging and disuse? Is it because each tiny little myofibril gets smaller… or is it because we lose myofibrils? In our new study, we addressed this in humans and mice. biorxiv.org/cgi/content/sh… Full breakdown of the findings in this thread 👇

@vanevery93 Thanks Derrick

More incredible findings from the @HornbergerLab !

I'm blown away by how well NotebookLM generated an infographic for our manuscript. It almost feels like cheating! As a scientist (not a graphic designer), it’s incredibly helpful to have a tool that produces visuals far better than I ever could. biorxiv.org/content/10.648…

8/ Take Home: Across species and conditions, the loss of myofibrils is a central and conserved mechanism of muscle fiber atrophy. Changes in myofibril CSA play a smaller, context-dependent role. Treatments for sarcopenia and disuse atrophy should target myofibril turnover.

7/ What about disuse? 10 days of hindlimb immobilization (IM) caused: ↓ Whole Muscle CSA ↓ Fiber CSA ↓ Myofibril Number / Fiber ↓ Myofibril CSA Disuse impacts both myofibril number and myofibril CSA and, importantly, aging blunted this response.