CD44 is a key player in non-alcoholic steatohepatitis

Patouraux, Stéphanie; Rousseau, Denis; Bonnafous, Stéphanie; Lebeaupin, Cynthia; Luci, Carmelo; Canivet, Clémence M.; Schneck, Anne-Sophie; Bertola, Adeline; Saint–Paul, Marie–Christine; Iannelli, Antonio; Gugenheim, Jean; Anty, Rodolphe; Tran, Albert; Bailly-Maître, Béatrice; Gual, Philippe

doi:10.1016/j.jhep.2017.03.003

Cited by 99 publications

(107 citation statements)

References 48 publications

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“…Oxidative Medicine and Cellular Longevity to a population of hepatologically healthy subjects (with only reflux disease not being treated) for several of the parameters evaluated. Specifically, NAFLD patients demonstrated greater BMI, body weight, insulin, HOMA-IR, total cholesterol, triglycerides, CRP, TNF-α, EGFR, CD-44, IL-18, IGF-II, IL-22, TGF-β, MMP-2, Endocan, HMGB-1, and TBARS, with the evidence, moreover, of lower average levels of vitamin D. This pathological picture fully reflects the data present in the scientific literature showing how patients affected by NAFLD are more exposed to oxidative stress, systemic inflammation, and endothelial dysfunction and have a higher blood level of inflammatory cytokines and fibrosis markers compared to healthy subjects, thus being more predisposed to all the pathologies supported by these harmful factors [47][48][49][50].…”

supporting

confidence: 78%

“…Furthermore, it would be able to act on hepatic stellate cells by inhibiting the extracellular signal-related kinase (ERK) activity, MAP/ERK kinase (MEK), and Raf phosphorylation, reducing the migration of leukocytes to the site of inflammation and reducing TGF-β-induced synthesis of type I procollagen as well as MMP-2 secretion [53]. These biological activities are responsible for controlling the inflammatory cascade, the deposition of fat accumulation in the hepatocytes, and the reduction of hepatic and extrahepatic deposition of fibrotic tissue [47][48][49][50]. An interesting point is represented by the fact that the improvement of the markers of disease worsening assessed is maintained well beyond the end of the treatment period.…”

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confidence: 99%

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Evaluation of the Effect Derived from Silybin with Vitamin D and Vitamin E Administration on Clinical, Metabolic, Endothelial Dysfunction, Oxidative Stress Parameters, and Serological Worsening Markers in Nonalcoholic Fatty Liver Disease Patients

Federico

Dallio

Masarone

et al. 2019

Oxidative Medicine and Cellular Longevity

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Nowadays, the nonalcoholic fatty liver disease represents the main chronic liver disease in the Western countries, and the correct medical therapy remains a big question for the scientific community. The aim of our study was to evaluate the effect derived from the administration for six months of silybin with vitamin D and vitamin E (RealSIL 100D®) on metabolic markers, oxidative stress, endothelial dysfunction, and worsening of disease markers in nonalcoholic fatty liver disease patients. We enrolled 90 consecutive patients with histological diagnosis of nonalcoholic fatty liver disease and 60 patients with diagnosis of reflux disease (not in therapy) as healthy controls. The nonalcoholic fatty liver disease patients were randomized into two groups: treated (60 patients) and not treated (30 patients). We performed a nutritional assessment and evaluated clinical parameters, routine home tests, the homeostatic model assessment of insulin resistance, NAFLD fibrosis score and fibrosis-4, transient elastography and controlled attenuation parameter, thiobarbituric acid reactive substances, tumor necrosis factor α, transforming growth factor β, interleukin-18 and interleukin-22, matrix metalloproteinase 2, epidermal growth factor receptor, insulin growth factor-II, cluster of differentiation-44, high mobility group box-1, and Endocan. Compared to the healthy controls, the nonalcoholic fatty liver disease patients had statistically significant differences for almost all parameters evaluated at baseline (p<0.05). Six months after the baseline, the proportion of nonalcoholic fatty liver disease patients treated that underwent a statistically significant improvement in metabolic markers, oxidative stress, endothelial dysfunction, and worsening of disease was greater than not treated nonalcoholic fatty liver disease patients (p<0.05). Even more relevant results were obtained for the same parameters by analyzing patients with a concomitant diagnosis of metabolic syndrome (p<0.001). The benefit that derives from the use of RealSIL 100D could derive from the action on more systems able to advance the pathology above all in that subset of patients suffering from concomitant metabolic syndrome.

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confidence: 78%

mentioning

confidence: 99%

Evaluation of the Effect Derived from Silybin with Vitamin D and Vitamin E Administration on Clinical, Metabolic, Endothelial Dysfunction, Oxidative Stress Parameters, and Serological Worsening Markers in Nonalcoholic Fatty Liver Disease Patients

Federico

Dallio

Masarone

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…For example, CD44, a type I transmembrane glycoprotein with over 20 different isoforms, has been demonstrated to be involved in liver disease and inflammation. 111,112 The canonical CD44 ligand is hyaluronic acid. Interactions between this ECM GAG and CD44 are known to facilitate migration of leukocytes to inflamed tissue, as well as the progression of inflammatory injury.…”

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confidence: 99%

The Matrisome, Inflammation, and Liver Disease

Dolin

Arteel

2020

Semin Liver Dis

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Chronic fatty liver disease is common worldwide. This disease is a spectrum of disease states, ranging from simple steatosis (fat accumulation) to inflammation, and eventually to fibrosis and cirrhosis if untreated. The fibrotic stage of chronic liver disease is primarily characterized by robust accumulation of extracellular matrix (ECM) proteins (collagens) that ultimately impairs the function of the organ. The role of the ECM in early stages of chronic liver disease is less well-understood, but recent research has demonstrated that several changes in the hepatic ECM in prefibrotic liver disease are not only present but may also contribute to disease progression. The purpose of this review is to summarize the established and proposed changes to the hepatic ECM that may contribute to inflammation during earlier stages of disease development, and to discuss potential mechanisms by which these changes may mediate the progression of the disease.

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“…En effet, chez les souris obèses, l'accumulation excessive de lipides dans le foie entraîne un déséqui-Les lipides jouent ainsi un rôle essentiel dans la mise en place de la réponse UPR et de la stéatose, puis dans son maintien vers des stades délétères.Suite à l'établissement de la stéatose qui vulnérabilise les hépatocytes, la mise en place de l'UPR « chronique » favoriserait la transition vers la stéatohépatite en aggravant les désordres métaboliques et en induisant des processus inflammatoires, de mort cellulaire et de la fibrose, les caractéristiques physiopathologiques de la stéatohépatite. Les patients atteints de NASH présentent en effet une inflammation qui est corrélée à la gravité histologique de leurs atteintes hépatiques[22]. Les biopsies de foie de ces patients révèlent également un nombre significativement plus élevé d'hépatocytes en apoptose (positifs au marquage TUNEL [terminal deoxynucleotidyl transferase dUTP nick end labeling], activation des caspases exécutrices de l'apoptose -caspases-3 et -7 -et augmentation de l'expression du récepteur de mort Fas) par rapport aux foies de patients minces ou stéatosiques[23].…”

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La réponse au stress du réticulum endoplasmique dans la physiopathologie des maladies chroniques du foie

et al. 2020

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La prévalence des maladies chroniques du foie ne cesse d’augmenter, du fait de la pandémie de l’obésité. Ces maladies s’étendent de la bégnine stéatose à la stéatopathie non alcoolique (NASH) qui peut évoluer vers le carcinome hépatocellulaire. Il n’existe pas de traitement pour ces maladies. La transition stéatose-NASH apparaît déterminante dans leur progression. Au cours de l’obésité, l’activation chronique de la réponse au stress du réticulum endoplasmique (RE) jouerait un rôle crucial dans cette transition, conduisant à la mort cellulaire, à l’inflammation et à l’aggravation des désordres métaboliques. Dans cette revue, nous discutons ces aspects et proposons que le ciblage de cette réponse au stress du RE puisse être pertinent dans la prise en charge thérapeutique de la NASH.

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CD44 is a key player in non-alcoholic steatohepatitis

Cited by 99 publications

References 48 publications

Evaluation of the Effect Derived from Silybin with Vitamin D and Vitamin E Administration on Clinical, Metabolic, Endothelial Dysfunction, Oxidative Stress Parameters, and Serological Worsening Markers in Nonalcoholic Fatty Liver Disease Patients

Evaluation of the Effect Derived from Silybin with Vitamin D and Vitamin E Administration on Clinical, Metabolic, Endothelial Dysfunction, Oxidative Stress Parameters, and Serological Worsening Markers in Nonalcoholic Fatty Liver Disease Patients

The Matrisome, Inflammation, and Liver Disease

La réponse au stress du réticulum endoplasmique dans la physiopathologie des maladies chroniques du foie

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