Relationship between Serum Cytokeratin-18, Control Attenuation Parameter, NAFLD Fibrosis Score, and Liver Steatosis in Nonalcoholic Fatty Liver Disease

Kosasih, Sumitro; Qin, Wong Zhi; Rani, Rafiz Abdul; Hamid, Nazefah Abd; Soon, Ngiu Chai; Shah, Shamsul Azhar; Yaakob, Yazmin; Ali, Raja Affendi Raja

doi:10.1155/2018/9252536

Cited by 16 publications

(16 citation statements)

References 42 publications

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“…Kosasih et al found that CK-18 played a critical role in progression of liver fibrosis. 26 On the other hand, Notch3 ameliorated cardiac fibrosis through inhibiting the expression of MMP9 and α-SMA. 27 Similar to these results, combination of silibinin with valsartan could inhibit renal fibrosis via suppression of MMP9, α-SMA and increase of CK-18 in TGF-β1-treated HK-2 cells.…”

Section: Discussionmentioning

confidence: 99%

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

Liu

Wang

Ding

et al. 2020

DDDT

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Background: Chronic kidney disease (CKD) has become a major public health issue. Meanwhile, renal fibrosis caused by diabetic nephropathy can lead to CKD, regardless of the initial injury. It has been previously reported that silibinin or valsartan could relieve the severity of renal fibrosis. However, the effect of silibinin in combination with valsartan on renal fibrosis remains unclear. Material and Methods: Proximal tubular cells (HK-2) were treated with TGF-β1 (5 ng/mL) to mimic in vitro model of fibrosis. The proliferation of HK-2 cells was tested by CCK-8. Epithelial-mesenchymal transition (EMT) and inflammation-related gene and protein expressions in HK-2 cells were measured by qRT-PCR and Western-blot, respectively. ELISA was used to test the level of TNF-αNF-A. Additionally, HFD-induced renal fibrosis mice model was established to investigate the effect of silibinin in combination with valsartan on renal fibrosis in vivo. Results: Silibinin significantly increased the anti-fibrosis effect of valsartan in TGF-β1-treated HK-2 cells via inhibition of TGF-β1 signaling pathway. Furthermore, silibinin significantly enhanced the anti-fibrosis effect of valsartan on HFD-induced renal fibrosis in vivo through inactivation of TGF-β1 signaling pathway. Conclusion: These data indicated that silibinin markedly increased anti-fibrosis effect of valsartan in vitro and in vivo. Thus, silibinin in combination with valsartan may act as a potential novel strategy to treat renal fibrosis caused by diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

Liu

Wang

Ding

et al. 2020

DDDT

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“…One such model is the diagnosis of steatosis index that includes the fatty liver index [ 31 ], hepatic steatosis index [ 32 ], SteatoTest [ 33 ], lipid accumulation product (LAP) [ 34 ], index of NASH (ION) [ 35 ], NAFLD liver fat score (LFS) [ 36 ], triglyceride-glucose index (TyG) [ 37 ], serum keratin 18 fragment (CK-18) [ 38 ], and visceral adiposity index (VAI) [ 39 ]. These index models’ diagnostic performance is acceptable; however, the performance is suboptimal when it comes to distinguishing steatosis grades [ 31 , 32 , 33 , 34 , 35 , 36 , 38 ]. Moreover, these indexes cannot differentiate among NAFLD individuals with and without NASH [ 40 ].…”

Section: Current Noninvasive Diagnostic Methodsmentioning

confidence: 99%

Nonalcoholic Fatty Liver Disease (NAFLD): Pathogenesis and Noninvasive Diagnosis

et al. 2021

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The global prevalence of nonalcoholic fatty liver disease (NAFLD) or metabolic associated fatty liver disease (MAFLD), as it is now known, has gradually increased. NAFLD is a disease with a spectrum of stages ranging from simple fatty liver (steatosis) to a severe form of steatosis, nonalcoholic steatohepatitis (NASH), which could progress to irreversible liver injury (fibrosis) and organ failure, and in some cases hepatocellular carcinoma (HCC). Although a liver biopsy remains the gold standard for accurate detection of this condition, it is unsuitable for clinical screening due to a higher risk of death. There is thus an increased need to find alternative techniques or tools for accurate diagnosis. Early detection for NASH matters for patients because NASH is the marker for severe disease progression. This review summarizes the current noninvasive tools for NAFLD diagnosis and their performance. We also discussed potential and newer alternative tools for diagnosing NAFLD.

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“…Several serum biomarkers, such as alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltranspeptidase, cytokeratin-18 and fibroblast growth factor 21, have been researched in some studies and their potential to serve as the biomarkers in clinical diagnosing of NAFLD have been mentioned. [14][15][16][17][18] Fetuin-A, also known as the 2-Heremans-Schmid glycoprotein, is a phosphorylated glycoprotein and a member of the fetuin group of serum binding proteins that are synthesized primarily by hepatocytes. 19 As an endogenous inhibitor of tyrosine kinase, fetuin-A can trigger insulin resistance in the target tissues, such as liver and skeletal muscle.…”

Section: Introductionmentioning

confidence: 99%

Systematic Review and Meta-analysis of Circulating Fetuin-A Levels in Nonalcoholic Fatty Liver Disease

Liu

Xiao

Zhao

et al. 2020

Journal of Clinical and Translational Hepatology

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Background and Aims Accumulated studies have reported the key role of circulating fetuin-A in the development and progression of nonalcoholic fatty liver disease (NAFLD) but the results have not been consistent. In this study, we performed a systematic review and meta-analysis to explore the relationship between circulating fetuin-A level and the development and classification of NAFLD. Methods The PubMed, EMBASE, and Cochrane Library databases were searched to obtain the potentially relevant studies up to May 2020. Standardized mean differences (SMD) and 95% confidence intervals of circulating fetuin-A levels were extracted and summarized. Sensitivity, subgroup analysis and meta-regression analysis were performed to investigate the potential heterogeneity. Association of circulating fetuin-A level with classification of NAFLD was also reviewed. Results A total of 17 studies were included, composed of 1,755 NAFLD patients and 2,010 healthy controls. Meta-analysis results showed that NAFLD patients had higher circulating fetuin-A level (SMD=0.43, 95% confidence interval [CI]: 0.22–0.63, p <0.001) than controls. Subgroup analysis indicated that circulating fetuin-A level was markedly increased in adult NAFLD patients (SMD=0.48, 95% CI: 0.24–0.72, p <0.001) and not in pediatric/adolescent patients compared to controls. Circulating fetuin-A level was markedly increased in ultrasound-proven NAFLD pediatric/adolescent patients (SMD=0.42, 95% CI: 0.12–0.72, p =0.007), other than in the liver biopsy-proven NAFLD pediatric/adolescent patients. Body mass index might be the influencing factor to the heterogeneity in adult patients. Circulating fetuin-A level was not associated with the classification of NAFL vs. nonalcoholic steatohepatitis (NASH). Whether the circulating fetuin-A level was associated with the development of fibrosis remains controversial. Conclusions Circulating fetuin-A level was significantly higher in NAFLD patients and was not associated with the classification of NAFL vs. NASH. Whether the circulating fetuin-A level was associated with the development of fibrosis remains controversial.

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Relationship between Serum Cytokeratin-18, Control Attenuation Parameter, NAFLD Fibrosis Score, and Liver Steatosis in Nonalcoholic Fatty Liver Disease

Cited by 16 publications

References 42 publications

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

<p>Silibinin Augments the Antifibrotic Effect of Valsartan Through Inactivation of TGF-β1 Signaling in Kidney</p>

Nonalcoholic Fatty Liver Disease (NAFLD): Pathogenesis and Noninvasive Diagnosis

Systematic Review and Meta-analysis of Circulating Fetuin-A Levels in Nonalcoholic Fatty Liver Disease

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