Peripheral immune cells in NAFLD patients: A spyhole to disease progression

Lin, Shuangzhe; Fan, Jian‐Gao

doi:10.1016/j.ebiom.2021.103768

Cited by 15 publications

(12 citation statements)

References 87 publications

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“…Gaining new insights into the role of innate immunity in MAFLD/NAFLD will enhance our understanding of disease pathogenesis, enable the identification of biomarkers able to select patients at risk, and distinguish those more likely to progress to cirrhosis, HCC and/or extrahepatic complications. Utilizing quantitative and molecular phenotypic changes in peripheral innate immune cells among MAFLD/NAFLD patients as a diagnostic tool to determine NASH progression and patient stratification appears as a promising noninvasive approach [ 99 ]. Innate immunity can be therapeutically manipulated, at the level of epigenetic modifiers, cellular metabolism and signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Innate immunity and nonalcoholic fatty liver disease

Kountouras

Kazakos

Kyrailidi

et al. 2023

aog

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Section: Discussionmentioning

confidence: 99%

Innate immunity and nonalcoholic fatty liver disease

Kountouras

Kazakos

Kyrailidi

et al. 2023

aog

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“…Clinical and epidemiological data discovered that 20 million people worldwide will eventually die of NAFLD-related liver disease and causes great health economic burden [25,26] . Multiple pathological processes have been identi ed as major culprits of NFALD, including oxidative damage, chronic in ammation, dyslipidemia and hepatocyte apoptosis [27,28] . Therefore, drugs or genes targeting the above processes may be an effective strategy of improving NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Cav3.2 deletion attenuates nonalcoholic fatty liver disease in mice

Dai

et al. 2023

Preprint

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Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases and also the main cause of liver cirrhosis and hepatocellular carcinoma. Cav3.2 channel is an important member of T-type calcium channel and plays a vital role in energy and metabolic balance. However, the effects of Cav3.2 on NFALD remain unclear. Here, we aimed to investigate the function of Cav3.2 channel in the development and progression of NAFLD. After 16 weeks on a high-fat diets (HFD), Cav3.2 knockout (Cav3.2 KO) improves hepatic steatosis, liver injury and metabolic syndrome in NAFLD mice model. We provided evidence that Cav3.2 KO inhibited HFD-induced hepatic oxidative damage, inflammation and hepatocyte apoptosis. In addition, Cav3.2 KO also attenuated the hepatic lipid accumulation, oxidative damage, inflammation and hepatocyte apoptosis in palmitic acid/oleic acid (PAOA)-treated primary hepatocytes. Further, Cav3.2 KO-mediated liver protection function were dependent on its interaction with CaMKII signaling. These results suggest that therapeutic approaches targeting Cav3.2 provide effective approaches for treating NAFLD.

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“…It is also possible to use flow cytometry analysis of blood leukocytes to discriminate NAFL and NASH patients. Both peripheral lymphocyte and myeloid cell subsets differ in terms of their abundance, activation, polarization or cell membrane markers [35, 36].…”

Section: Discussionmentioning

confidence: 99%

Hepatic MCPIP1 protein levels are reduced in NAFLD patients and are predominantly expressed in cholangiocytes and liver endothelium

Pydyn

Kadłuczka

Major

et al. 2022

Preprint

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Nonalcoholic fatty liver disease (NAFLD) is characterized by the excessive accumulation of fat in hepatocytes. NAFLD can range from simple steatosis to the aggressive form called nonalcoholic steatohepatitis (NASH), which is characterized by both fatty liver and liver inflammation. Without proper treatment, NAFLD may further progress to life-threatening complications, such as fibrosis, cirrhosis or liver failure. Monocyte chemoattractant protein-induced protein 1 (MCPIP1, alias Regnase 1) is a negative regulator of inflammation, acting through the cleavage of transcripts coding for proinflammatory cytokines and the inhibition of NFkB activity. In this study, we investigated MCPIP1 expression in the liver and peripheral blood mononuclear cells (PBMCs) collected from a cohort of 36 control and NAFLD patients hospitalized due to bariatric surgery or primary inguinal hernia laparoscopic repair. Based on liver histology data (H&E and Oil Red O staining), 12 patients were classified into the nonalcoholic fatty liver (NAFL) group, 19 into the NASH group and 5 into the control (non-NAFLD) group. Biochemical characterization of patient plasma was followed by expression analysis of genes regulating inflammation and lipid metabolism. The MCPIP1 protein level was reduced in the livers of NAFL and NASH patients in comparison to non-NAFLD control individuals. Additionally, in all groups of patients, immunohistochemical staining showed that the expression of MCPIP1 was higher in the portal fields and bile ducts in comparison to the liver parenchyma and central vein. The liver MCPIP1 protein level negatively correlated with hepatic steatosis but not with patient BMI or any other analyte. The MCPIP1 level in PBMCs did not differ between NAFLD patients and control patients. Similarly, in patients PBMCs there were no differences in the expression of genes regulating beta-oxidation (ACOX1, CPT1A, and ACC1) and inflammation (TNF, IL1B, IL6, IL8, IL10, and CCL2), or transcription factors controlling metabolism (FAS, LCN2, CEBPB, SREBP1, PPARA, and PPARG). We have demonstrated that MCPIP1 protein levels are reduced in NAFLD patients, but further research is needed to investigate the specific role of MCPIP1 in NAFL initiation and the transition to NASH.

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Peripheral immune cells in NAFLD patients: A spyhole to disease progression

Cited by 15 publications

References 87 publications

Innate immunity and nonalcoholic fatty liver disease

Innate immunity and nonalcoholic fatty liver disease

Cav3.2 deletion attenuates nonalcoholic fatty liver disease in mice

Hepatic MCPIP1 protein levels are reduced in NAFLD patients and are predominantly expressed in cholangiocytes and liver endothelium

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