Laboratory of Exercise and Health - ETH Zürich

Researchers discover trigger of tendon disease Overuse of our tendons can cause painful medical conditions for which only limited treatment options exist. Researchers have now deciphered an important molecular mechanism that triggers these problem...

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Excited to announce that registration is officially open for #METPHYS2026!

All meeting details can be found here:
www.sablesys.com/metphys-the-...

This work was a true team effort. Huge thanks to all co-authors and collaborators!!!

Why does this matter in vivo? Using a synergist ablation overload, we show that tendon maladaptation develops over time. Genetic inhibition of HIF1α in tendon fibroblasts preserves tendon structure and mechanics. This supports HIF1α-regulated pathways as potential therapeutic entry point. (7/8)

But, what triggers HIF1α? Mechanical overload. In vitro, tendon fibroblasts show a strain-dependent increase in HIF1α activation. Ex vivo, HIF1α activation emerges only once loading exceeds a damage threshold, indicating damage-associated activation, even under normal oxygen conditions. (6/8)

By genetically decoupling vascular recruitment from HIF1α activation (via VEGFA-dependent mechanisms), we show that tendon degeneration occurs independently of angiogenesis, while vascular invasion is tightly coupled to myelinated nerve ingrowth. (5/8)

To investigate causality, we generated a tendon fibroblast–specific mouse model with chronic HIF1α activation. HIF1α activation alone was sufficient to drive ECM disorganization, mechanical dysfunction, hypercellularity, and neurovascular ingrowth, hallmark features of human tendinopathy. (4/8)

Quantitative proteomics further uncovered pathological collagen remodeling, including increased pyridinoline (↑ PYD) crosslinking and altered collagen composition, helping explain why tendinopathic tendons become mechanically compromised. (3/8)

We started with clinical observations. Analyzing human tendinopathic samples, we asked which molecular pathways are altered in disease. Using immunofluorescence and integrative omics, we found strong enrichment of HIF1α signaling in both diseased long head of biceps and rotator cuff tear tendons.

What started off with some nice discussions with @Jess Snedeker turned into a longlasting collaboration, spearheaded by the amazing @greta moschini and a lot of awesome collaborations. 👇

HIF1α gates tendon response to overload and drives tendinopathy independently of vascular recruitment HIF1α activation promotes tendinopathy, and its inhibition prevents overload-induced maladaptation, suggesting therapeutic potential.

Healthy tendons do not contain an extensive #vascular network, so why would I be interested? Well, vascular ingrowth is a hallmark of #tendinopathy! 👇 Look at what Greta discovered! #snedekerlab #debocklab

www.science.org/doi/10.1126/...

Today, we see the fruit of 5+ years of teamwork. We have built a map of the neutrophil compartment (mostly in mice - but also humans). It provides a biological structure that focuses on a single immune cell lineage to discover the many ways in which neutrophils "interpret" physiology.

Goobye @viola Vogel! Prioneer in bio-physics, bio-engineering and leading lady of DHEST…#rolemodels #womeninscience #eth

Thanks @britta Engelhardt for serving the @ssmvr.bsky.social as our president forr many years!

1/10/2015-1/10/2025 🎂
10 years @ethz.ch #timeflies
10 years of great people and exciting science
thanks to all people who were part of the lab, who collaborated with us, and who made those years a fantastic time!

Good luck Emm! Sad to see you leaving us but hope to stay in touch. Enjoy Basel!

Unfortunately similar experience for me. I left X but Bluesky currently less than 10% of visibility…

Data can be freely explored at shiny.debocklab.hest.ethz.ch/Turiel-et-al/

Single-cell compendium of muscle microenvironment in peripheral artery disease reveals altered endothelial diversity and LYVE1+ macrophage activation Nature Cardiovascular Research - Using single-cell and spatial transcriptomics on muscle samples from non-ischemic patients and patients with peripheral artery disease (PAD), Turiel et al. identify...

Great and unique resource for those who are interested in studying peripheral artery disease mechanisms 👇. Congratulations to Guillermo Turiel and huge thanks to all our collaborators @ethz.ch and Kantonsspital Baden. #PAD #endothelialcells #peripheralarterydisease
rdcu.be/eGpZI

On my way to #BeNeVBO, taking the train to Leuven as I have done for many years!

As scientists, we all need to speak up. Thanks, Guillermo Oliver and @labonnelab.bsky.social for all the science advocacy. 🔬

But we ALL need to be telling our friends, family, and neighbors how important science is. Educate them about the medical cures that came from basic discoveries.

#science

Returning home from a fantastic gordon Research Confernce in #angiogenesis. Thanks @karinayaniv.bsky.social and @anne eichmann for the splendid organization! Couldn’t leaave the USA without a big hug to Gillian and Jing ❤️.

Liraglutide improves peripheral perfusion and markers of angiogenesis and inflammation in people with type 2 diabetes and peripheral artery disease: An 18‐month follow‐up of a randomized clinical trial Aims In a six-month randomized clinical trial, improved peripheral perfusion has been shown with liraglutide, associated with favourable vascular effects in people with type 2 diabetes and periphera...

The emerging vascular biology of GLP-1 medicines in people with #T2D and PAD dom-pubs.onlinelibrary.wiley.com/doi/full/10....

Excited to be part of the first #Hi-TAC symposium in beautiful Heidelberg. Team efforts in angiocardioscience will make the difference!

Context-dependent response of endothelial cells to PIK3CA mutation Cancer mutations in the PIK3CA gene cause congenital disorders. The endothelium is among the most frequently affected tissues in these disorders, displaying aberrant vascular overgrowth in the form of...

We are excited to share our work on Context-dependent response of endothelial cells to PIK3CA mutation. A tour the force of many; thank you all for your invaluable contribution. @aangulou.bsky.social @ruibenedito.bsky.social @debocklab.bsky.social @sandradcastillo.bsky.social
bit.ly/4blKSqa

HIF1α gates tendon response to overload and drives tendinopathy independently of vascular recruitment Tendons are mostly avascular dense connective tissues that link muscles to bones, withstanding some of the highest mechanical stresses in the body. Mechanical overload and tissue hypervascularity are ...

When you're working in an engineering school you end up talking about mechanics ;-). Together with Jess Snedeker-lab, we embarked on studying the molecular mechanisms underlying #tendinopathy. Currently revising the comments of the reviewers, but you can read it now:
www.biorxiv.org/content/10.1...

Cellular crosstalk in skeletal muscle? A surprising role for mast cells? Histamine as a signal transducer during exercise? Check out the story in @cp-cellmetabolism.bsky.social 🧵

@wimderave.bsky.social, @ugent-fge.bsky.social, @fwovlaanderen.bsky.social

www.sciencedirect.com/science/arti...

#EVBOSummerSchool 2025: Please help spread the news!
10-11 June 2025 | Biomedicum Helsinki, Finland
Registration will open soon. Stay tuned!
The summer school will be preceded by the excellent and free-of-charge Wihuri Research Symposium on Cardiovascular Biology!

More info https://buff.ly/42I9fvY

Proud about this one! Together with EA Richter ending up twice in the same issue of @cp-cellmetabolism.bsky.social ! #luck or my lab is great ;-). Thanks @wimderave.bsky.social and Zelzer labs for the nice collaborations!
authors.elsevier.com/sd/article/S...
authors.elsevier.com/c/1kZR45WXUl...

Accepted only few days before the end of 2024, happy to share it at the start of 2025. Hoping for a happy, healthy and peaceful year for ALL!! #skeletalmuscle #FAPs #osteoarthritis and #worldpeace

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