Project: MOlecular mechanisms of cellular DEath and Life decisions in Inflammation, Degeneration and Infection
2018-01-01 – 2021-12-31
- Abstract
The research program on Molecular mechanisms of cellular DEath and Life decisions in Inflammation, Degeneration and Infection (MODEL-IDI) aims at performing fundamental research on the biology of cell death modalities, cell survival regulation and their consequences on the onset and/or progression of diseases. The program aims at linking the discoveries obtained in vitro on the molecular regulation of cell death and inflammation to their in vivo physiological relevance by making use of chemical tool compounds and experimental models of diseases, such as diabetes type I & II, hepatotoxicity and liver cancer,
atherosclerosis and neurodegenerative diseases.
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- Journal Article
- open access
A guide to the expanding field of extracellular vesicles and their release in regulated cell death programs
(2023) FEBS JOURNAL. -
- Journal Article
- A1
- open access
Systematic compositional analysis of exosomal extracellular vesicles produced by cells undergoing apoptosis, necroptosis and ferroptosis
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- Journal Article
- A1
- open access
Ferroptosis contributes to multiple sclerosis and its pharmacological targeting suppresses experimental disease progression
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- Journal Article
- A1
- open access
Ferroptosis and pyroptosis signatures in critical COVID-19 patients
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- Journal Article
- A1
- open access
Inhibition of RIPK1 kinase does not affect diabetes development : beta-cells survive RIPK1 activation
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- Journal Article
- A1
- open access
From PERK to RIPK1 : design, synthesis and evaluation of novel potent and selective necroptosis inhibitors
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- A1
- open access
LC3-independent autophagy is vital to prevent TNF cytotoxicity
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- Journal Article
- A1
- open access
Death by TNF : a road to inflammation
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- Journal Article
- A1
- open access
Molecular mechanisms of nemorosone-induced ferroptosis in cancer cells
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- Journal Article
- A1
- open access
RIPK1 kinase-dependent inflammation and cell death contribute to the pathogenesis of COPD