Invitation to Participate in the Lemanic Life Sciences Hackathon 2025

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https://www.epfl.ch/schools/sv/lemanic-life-sciences-hackathon-2025

We are organizing the 2nd iteration of the Lemanic Life Sciences Hackathon 2025. The goal is bringing together computational scientists and clinicians/biologists to collaborate on data science-related projects. The format is unique: we independently recruit both projects and participants (“hackers”), then match them afterwards on interests. Our first edition last year was a great success with almost 100 participants, many sponsors and three deserving winners. The next iteration will be in April 2025.

At this stage, we are particularly looking for exciting challenges that the participants could tackle – it’s easier for us to find strong computer scientists & quantitative participants. Thus, I’m reaching out to ask if you (or your students) have any interesting challenges that come to your mind? Past projects involved Aberrant speech recognition for Parkinson’s Patients, creating tools for biodiversity identification in the field, decoding EMG, Generative modeling for designing antibiotics-resistant phage…. 

More information on the hackathon is available here: https://www.epfl.ch/schools/sv/lemanic-life-sciences-hackathon-2025/

Alexander Mathis https://mathislab.org

CIG Seminars Spring 2025 Program

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Monday 12:15, Génopode, auditorium B (or to be announced)

Monday January 20, 2025 (Joint CIG / DBC Seminar)
Julien Gagneur,
Technical University of Munich (DE)
«TBA»
Hosts: Maria Cristina Gambetta & Giovanni Ciriello

Monday January 27, 2025
Jagannathan Madhav,
ETHZ, Zurich (CH)
«TBA»
Host: Maria Cristina Gambetta

Monday February 10, 2025
Caren Norden,
Gulbenkian Institute for Molecular Medicine, Lisbonne (PT)
«TBA»
Host: Nadine Vastenhouw

Monday February 17, 2025
Stefanie Jonas,
ETHZ, Zurich (CH)
«TBA»
Host: Aleksandar Vjestica

Monday February 24, 2025
Richard Merrill,
Ludwig-Maximilians Universität Munchen (DE)
«TBA»
Host: Johannes Larsch

Monday March 10, 2025
Sundaresan Venkatesan,
University of California, Davis (USA)
«TBA»
Host: Christian Fankhauser

Monday March 17, 2025
Simon Bekker-Jensen,
University of Copenhagen (DK)
«TBA»
Host: David Gatfield

Monday March 24, 2025
Arnaud Hubstenberger,
Université Côte-d’Azur, Nice (FR)
«TBA»
Hosts: Nadine Vastenhouw & Jean-Yves Roignant

Monday April 28, 2025
Catherine Peichel,
University of Bern (CH)
«TBA»
Host: Johannes Larsch

Monday May 19, 2025
Maude Baldwin,
Max Planck Institute, Martinsried (DE)
«TBA»
Host: Johannes Larsch

Monday June 30, 2025
Maria Antonietta Tosches,
Columbia University, New York (USA)
«TBA»
Host: Richard Benton

Pharmacol Res, co-auth.: W.Wahli

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PPARβ/δ prevents inflammation and fibrosis during diabetic cardiomyopathy

Adel Rostami 1, Xavier Palomer 2, Javier Pizarro-Delgado 1, Emma Barroso 1, Brenda Valenzuela-Alcaraz 3, Fátima Crispi 3, J Francisco Nistal 4, María A Hurlé 5, Raquel García 5, Walter Wahli 6, Manuel Vázquez-Carrera 7

Affiliations Expand

Free article

Abstract

Diabetic cardiomyopathy (DCM) is a specific type of myocardial disease that often develops in patients suffering from diabetes, which has become the foremost cause of death among them. It is an insidious multifactorial disease caused by complex and partially unknown mechanisms that include metabolic dysregulation, local inflammation, fibrosis, and cardiomyocyte apoptosis. Despite its severity and poor prognosis, it often goes undiagnosed, and there are currently no approved specific drugs to prevent or even treat it. Peroxisome proliferator-activated receptor (PPAR)β/δ is a key metabolic regulator that has been proposed as a potential target for DCM due to its pleiotropic anti-inflammatory properties. Diabetes was induced by multiple low-dose streptozotocin (STZ) administration in wild-type and PPARβ/δ knockout male mice treated with the PPARβ/δ agonist GW0742 or vehicle. Human cardiomyocytes (AC16) and mouse atrial myocytes (HL-1) exposed to hyperglycemia and treated with PPARβ/δ agonists were also used. PPARβ/δ deletion in mice negatively impacted cardiac morphology and function, which was accompanied by interstitial fibrosis and structural remodeling of the heart. This phenotype was further exacerbated in knockout diabetic mice. At the molecular level, PPARβ/δ suppression resulted in increased expression of pro-inflammatory and pro-fibrotic markers. Some of these markers were also induced by diabetes in wild-type mice and were exacerbated in diabetic knockout mice. The activity of the transcription factors nuclear factor κB (NF-κB) and activator protein-1 (AP-1) correlated with most of these changes. Remarkably, PPARβ/δ activation partially prevented inflammation and fibrosis in the heart, as well as cardiac atrophy, induced during diabetes in mice, and also in cultured cardiomyocytes exposed to hyperglycemia. Finally, our results suggest that the beneficial effects of PPARβ/δ activation are mediated by the inhibition of mitogen-activated protein kinases (MAPK) activity and subsequent downregulation of the transcriptional activities of NF-κB and AP-1. Overall, the data suggest that PPARβ/δ agonists might be useful in preventing inflammation and fibrosis progression in DCM.

ReviewProg Lipid Res, auth.: W.Wahli

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Lipid sensing by PPARα: Role in controlling hepatocyte gene regulatory networks and the metabolic response to fasting

Anne Fougerat 1, Justine Bruse 2, Arnaud Polizzi 2, Alexandra Montagner 3, Hervé Guillou 2, Walter Wahli 4

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Free article

Abstract

Peroxisome proliferator-activated receptors (PPARs) constitute a small family of three nuclear receptors that act as lipid sensors, and thereby regulate the transcription of genes having key roles in hepatic and whole-body energy homeostasis, and in other processes (e.g., inflammation), which have far-reaching health consequences. Peroxisome proliferator-activated receptor isotype α (PPARα) is expressed in oxidative tissues, particularly in the liver, carrying out critical functions during the adaptive fasting response. Advanced omics technologies have provided insight into the vast complexity of the regulation of PPAR expression and activity, as well as their downstream effects on the physiology of the liver and its associated metabolic organs. Here, we provide an overview of the gene regulatory networks controlled by PPARα in the liver in response to fasting. We discuss impacts on liver metabolism, the systemic repercussions and benefits of PPARα-regulated ketogenesis and production of fibroblast growth factor 21 (FGF21), a fasting- and stress-inducible metabolic hormone. We also highlight current challenges in using novel methods to further improve our knowledge of PPARα in health and disease.