Fibrose

Résumé

thumb|Fibrose cardiaque (en jaune à gauche). La fibrose (synonyme de sclérose) survient à la suite d'une destruction substantielle des tissus ou lorsqu'une inflammation a lieu à un endroit où les tissus ne se régénèrent pas. L'exsudat (protéines plasmatiques ayant migré vers le milieu interstitiel lors de la réaction inflammatoire) n'est pas réabsorbé ou ne l'est pas suffisamment (par la lymphe) et s'agence avec le tissu conjonctif dans le milieu interstitiel. Face à des dommages tissulaires majeurs, la cicatrisation est la seule issue. Fibrose pulmonaire Fibrose pulmonaire Altération chronique et progressive du tissu pulmonaire (parenchyme) dont les alvéoles sont enserrées et étouffées par des fibres. Fibrose hépatique Fibrose hépatique Tissu fibreux se développant là où les cellules hépatiques ont été détruites. Quand la fibrose s'étend, elle peut provoquer le développement d'une cirrhose. Le diagnostic et l'évaluation du degré de la fibrose hépatique ont

Source officielle

https://fr.wikipedia.org/wiki/Fibrose

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The course covers in detail the interactions of cancer cells with their environment with an emphasis on tumor-angiogenesis, inflammation, adaptive and innate immunity and cancer-induced immune suppression. Additional topics are cancer metabolism, cancer stem cells and metastasis.

The course introduces the main classes of biomaterials used in the biomedical field. The interactions with biological environment are discussed and challenges highlighted. State of the art examples per type of material are discussed. Students will generate a biomaterial and study cell compatibility.

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Dissecting the role of the mitochondrial carrier SLC25A47

Nadia Bresciani

Transporters of the SLC25 mitochondrial carrier superfamily bridge cytoplasmic and mitochondrial metabolism by channeling metabolites across mitochondrial membranes and are pivotal for metabolic homeostasis. Despite their physiological relevance as gatekeepers of cellular metabolism, most of the SLC25 family members remain uncharacterized. During my PhD studies, I investigated the function of SLC25A47, an orphan carrier uniquely expressed in hepatocytes. We used a murine loss-of-function (LOF) model to unravel the role of this transporter in mitochondrial and hepatic homeostasis. Slc25a47hep-/- mice displayed a wide variety of metabolic abnormalities, as a result of sustained energy deficiency in the liver originating from impaired mitochondrial respiration in this organ. This mitochondrial phenotype was associated with a robust activation of the mitochondrial stress response (MSR) in the liver, which in turn, induced the secretion of several mitokines, amongst which FGF21 played a preponderant role in the translation of the effects of the MSR on systemic physiology. To dissect the FGF21-dependent and -independent physiological changes induced by the loss of Slc25a47, we generated a double Slc25a47-Fgf21 LOF mouse model, and demonstrated that several aspects of the hypermetabolic state were entirely driven by hepatic secretion of FGF21. On the other hand, the metabolic fuel inflexibility induced by loss of Slc25a47 could not be rescued by genetic removal of Fgf21. Finally, we challenged Slc25a47hep-/- mice with high-fat high-sucrose (HFHS) diet and observed the development of liver fibrosis.Collectively, the data presented in this thesis show that SLC25A47 is a novel determinant of hepatic metabolism and place this carrier at the center of mitochondrial homeostasis.

EPFL2022

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Renal tubular arginase-2 participates in the formation of the corticomedullary urea gradient and attenuates kidney damage in ischemia-reperfusion injury in mice

Camille Ansermet, Jean-Luc Barras, Nicolas Dattner, Dmitri Firsov, Hikari Ananda Infinity Yoshihara

Aim Arginase 2 (ARG2) is a mitochondrial enzyme that catalyses hydrolysis ofl-arginine into urea andl-ornithine. In the kidney, ARG2 is localized to the S3 segment of the proximal tubule. It has been shown that expression and activity of this enzyme are upregulated in a variety of renal pathologies, including ischemia-reperfusion (IR) injury. However, the (patho)physiological role of ARG2 in the renal tubule remains largely unknown. Methods We addressed this question in mice with conditional knockout ofArg2in renal tubular cells (Arg2(lox/lox)/Pax8-rtTA/LC1 or, cKO mice). Results We demonstrate that cKO mice exhibit impaired urea concentration and osmolality gradients along the corticomedullary axis. In a model of unilateral ischemia-reperfusion injury (UIRI) with an intact contralateral kidney, ischemia followed by 24 hours of reperfusion resulted in significantly more pronounced histological damage in ischemic kidneys from cKO mice compared to control and sham-operated mice. In parallel, UIRI-subjected cKO mice exhibited a broad range of renal functional abnormalities, including albuminuria and aminoaciduria. Fourteen days after UIRI, the cKO mice exhibited complex phenotype characterized by significantly lower body weight, increased plasma levels of early predictive markers of kidney disease progression (asymmetric dimethylarginine and symmetric dimethylarginine), impaired mitochondrial function in the ischemic kidney but no difference in kidney fibrosis as compared to control mice. Conclusion Collectively, these results establish the role of ARG2 in the formation of corticomedullary urea and osmolality gradients and suggest that this enzyme attenuates kidney damage in ischemia-reperfusion injury.

WILEY2020

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Magnetic resonance elastography for the noninvasive staging of liver fibrosis

Najat Salameh

The purpose of our study was to prospectively compare the success rate and diagnostic accuracy of magnetic resonance elastography, ultrasound elastography, and aspartate aminotransferase to platelets ratio index (APRI) measurements for the noninvasive staging of fibrosis in patients with chronic liver disease.

2008

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