Hepatic Fibrosis

Friedman, Scott L.

doi:10.1002/9781119251316.ch10

Cited by 5 publications

(41 citation statements)

References 194 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…10 In the normal liver, fibril-forming collagens (type I, type III, type V, and type XI collagens) can be found in the capsule, in large vessels, and the portal regions. 3 Only small amounts of type I and type III collagens are present in the subendothelial space. Additional components of the normal ECM include glycosaminoglycans and proteoglycans (hyaluronan, fibronectin, tenascin, or laminin) and other collagens (types VI, XIV, and XVIII).…”

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

“…3 In human patients and rodent models of liver disease, early deposition of ECM components takes place along the subendothelial space. 2,3 In humans, von Willebrand's factor expression is used as a marker of this process and expression of von Willebrand's factor, varying in distribution from diffuse to periportal, also was found in 69% of dogs with chronic liver disease. 11 The main mechanism of fibrogenesis is believed to be the activation of myofibroblast precursor cells, which results in the progressive deposition of ECM.…”

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

“…The fibrotic liver contains increased amounts of fibrillary collagens (types I, III, and V), nonfibrillary collagens (types IV and VI), and glycosaminoglycans and proteoglycans (eg, fibronectin, tenascin and laminin, perlecan, decorin, aggrecan, and fibromodulin). 1,3 During ECM accumulation, cross-linking of matrix proteins occurs. In advanced fibrosis, this feature has been proposed to render the ECM more resistant to degradation.…”

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

“…17 The transdifferentiation of quiescent HSCs to myofibroblasts is a multi-step process that involves cytokines, chemokines, growth factors, reactive oxygen species (ROS), and apoptotic bodies derived from hepatocytes (Fig 1). 3,[18][19][20] In the early phase of activation, the HSC acquires responsiveness to cytokine stimuli by exposure to fibronectin or apoptotic bodies derived from damaged hepatocytes. 18 In the next phase, cytokines and growth factors, produced by neighboring cells such as liver resident macrophages (Kupffer cells), hepatocytes, endothelial cells, lymphocytes, and platelets, bind to specific receptors on the HSC membrane.…”

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

“…[1][2][3] In a fibrotic liver, the total collagen content is 3-to 10-fold higher than normal. 3 Development of hepatic fibrosis is an important step in the progression of many liver diseases, and it has been shown to have prognostic implications in human patients. 4,5 As is the case with human patients, hepatic fibrosis can contribute to the development of portal hypertension and acquired portosystemic collateral blood vessels in dogs.…”

mentioning

confidence: 99%

See 4 more Smart Citations

Hepatic Fibrosis in Dogs

Eulenberg

Lidbury

2017

Veterinary Internal Medicne

View full text Add to dashboard Cite

Hepatic fibrosis is commonly diagnosed in dogs, often as a sequela to chronic hepatitis (CH). The development of fibrosis is a crucial event in the progression of hepatic disease that is of prognostic value. The pathophysiology of hepatic fibrosis in human patients and rodent models has been studied extensively. Although less is known about this process in dogs, evidence suggests that fibrogenic mechanisms are similar between species and that activation of hepatic stellate cells is a key step. Diagnosis and staging of hepatic fibrosis in dogs requires histopathological examination of a liver biopsy specimen. However, performing a liver biopsy is invasive and assessment of fibrotic stage is complicated by the absence of a universally accepted staging scheme in veterinary medicine. Serum biomarkers that can discriminate among different fibrosis stages are used in human patients, but such markers must be more completely evaluated in dogs before clinical use. When successful treatment of its underlying cause is feasible, reversal of hepatic fibrosis has been shown to be possible in rodent models and human patients. Reversal of fibrosis has not been well documented in dogs, but successful treatment of CH is possible. In human medicine, better understanding of the pathomechanisms of hepatic fibrosis is leading to the development of novel treatment strategies. In time, these may be applied to dogs. This article comparatively reviews the pathogenesis of hepatic fibrosis, its diagnosis, and its treatment in dogs.

show abstract

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

Section: Hepatic Fibrosis and Myofibroblastsmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Hepatic Fibrosis in Dogs

Eulenberg

Lidbury

2017

Veterinary Internal Medicne

View full text Add to dashboard Cite

show abstract

Three-dimensional visualization of the microvasculature of bile duct ligation-induced liver fibrosis in rats by x-ray phase-contrast imaging computed tomography

Xuan

Zhao

et al. 2015

Sci Rep

View full text Add to dashboard Cite

X-ray phase-contrast imaging (PCI) can substantially enhance contrast, and is particularly useful in differentiating biological soft tissues with small density differences. Combined with computed tomography (CT), PCI-CT enables the acquisition of accurate microstructures inside biological samples. In this study, liver microvasculature was visualized without contrast agents in vitro with PCI-CT using liver fibrosis samples induced by bile duct ligation (BDL) in rats. The histological section examination confirmed the correspondence of CT images with the microvascular morphology of the samples. By means of the PCI-CT and three-dimensional (3D) visualization technique, 3D microvascular structures in samples from different stages of liver fibrosis were clearly revealed. Different types of blood vessels, including portal veins and hepatic veins, in addition to ductular proliferation and bile ducts, could be distinguished with good sensitivity, excellent specificity and excellent accuracy. The study showed that PCI-CT could assess the morphological changes in liver microvasculature that result from fibrosis and allow characterization of the anatomical and pathological features of the microvasculature. With further development of PCI-CT technique, it may become a novel noninvasive imaging technique for the auxiliary analysis of liver fibrosis.

show abstract