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Functions of the Liver
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Other specialized cells are also found within the sinusoids. These include endothelial, Pit and Ito cells (specific natural killer cells). Endothelial cells line the vasculature and are fenestrated, allowing molecular exchange between the hepatocyte and the space of Disse. Pitt cells are mobile lymphocytes attached to the endothelium and play a defensive role against infection and tumour cells. Ito cells contain fat and also store vitamin A and other retinoids. The space of Disse lies between the endothelial cells of the sinusoid and the hepatocyte membrane. Collagen, fibronectin and proteoglycans are found within this space, which is also important for lymphatic transport.
Kinetics of Blood to Cell Uptake of Radiotracers*
Published in Lelio G. Colombetti, Biological Transport of Radiotracers, 2020
James B. Bassingthwaighte, Bernd Winkle
The cellular uptake of glucose and rubidium was estimated by Goresky et al.33 for the liver. A model of the special anatomical situation of a single sinusoid was formulated: the blood flows through the sinusoid which is surrounded by the extracellular space of Disse. The extracellular space is freely accessible to solutes through the fenestrated sinusoidal endothelium which means that exchange is only limited by flow. The barrier limitation for Rb and glucose occurs at the hepatocyte membrane. The conservation equation was solved for the solute concentration in the sinusoid and in the cell for unsequestered material. The extracellular concentration equals the sinusoid concentration multiplied by the partition coefficient of the substance in the space of Disse. An analytical solution was obtained for the Dirac delta function as impulse input by applying the Laplace transformation.
Structural Organization of the Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
As regards the function of the extracellular matrix, bundles of collagen fibers are thought to form the intralobular structural frame anchoring and supporting cells in lobular parenchyma. The absence of continuous basement membrane in the space of Disse is conducive to facilitate the rapid metabolic exchange between hepatocytes and plasma. Although the functional significance of the fibronectin found in the perisinusoidal space is not clear, it may serve the same function as the fibronectin deposited in the early stage of development: that of a primary extracellular matrix, which is less restrictive than a basement membrane in terms of filtration (Martinez-Hernandez, 1984).
Gut non-bacterial microbiota contributing to alcohol-associated liver disease
Published in Gut Microbes, 2021
Wenkang Gao, Yixin Zhu, Jin Ye, Huikuan Chu
Once the intestinal barrier collapses, the liver becomes the first organ to encounter intestinal products, which makes it susceptible to pathological changes.32,33 Liver sinusoidal endothelial cells (LSECs), a major member of the hepatic barrier, provide a second line of defense against gut-derived antigens and inflammatory factors.34 LSECs are highly fenestrated cells (Figure 1(c)). The diameters of transcellular pores on LSECs are 50 ~ 200 nm and these LSECs usually act as a dynamic filter under physiological conditions.35,36 For example, small molecules, such as chylomicron remnants, plasma proteins, and lipoproteins, can cross fenestrae and reach the space of Disse for uptake and utilization by hepatocytes and HSCs.37 Furthermore, LSECs can remove recycled waste products and toxicants, including enteric viruses,38,39 bacteriophages,40 lipopolysaccharides (LPS),41 and immune complexes.42 LSECs can also maintain the quiescent state of hepatic stellate cells, induce hepatic immune tolerance and exert an anti-inflammatory effect.43,44 Due to the existence of the second line of defense, the sole injury of the intestinal barrier is unlikely to lead to significant liver damage, which has been confirmed experimentally in the previous studies.32,33
Advances in the clinical use of collagen as biomarker of liver fibrosis
Published in Expert Review of Molecular Diagnostics, 2020
Steffen K. Meurer, Morten A. Karsdal, Ralf Weiskirchen
The hallmark of liver fibrosis is the formation and deposition of excess fibrous connective tissue, leading to progressive architectural tissue remodeling [14,15]. Although the triggering factors of hepatic fibrosis are manifold (genetic disorders, viral infection, alcohol abuse, autoimmune attacks, metabolic disorders, cholestasis, venous obstruction, parasite infections, and others), the principal mechanisms leading to the onset of fibrogenesis are the same. The pathological sequence of fibrosis is initiated by parenchymal cell destruction that induces an inflammatory response, in which non-parenchymal cells and resident immune cells are triggered to release a large variety of inflammatory and pro-fibrogenic mediators within the liver tissue [16]. This in turn provokes the activation of hepatic stellate cells (HSC) that transit to matrix-producing myofibroblasts (MFB) [14,15]. At the same time, it comes to proliferation of the bile ducts and elevated production and deposition of different collagen types in the space of Disse, liver parenchyma, and the portal tracts Figure 1.
Therapeutic targets for liver regeneration after acute severe injury: a preclinical overview
Published in Expert Opinion on Therapeutic Targets, 2020
Hidenobu Kojima, Kojiro Nakamura, Jerzy W. Kupiec-Weglinski
Various clinical and basic studies imply the relationships between liver age and liver tissue regeneration. Younger donor clinical cohort (<30 years) showed significantly higher liver regeneration rates in volume than the older donor group (>50 years) at 1 week after living donor partial liver transplantation (LDLT), although there was no difference in the liver regeneration rate between those groups at 1 month after LDLT [73,74]. Cumulative recipient survival rate was also significantly higher in the younger donor group (<20 years) compared with the older donor group (20 years or above) after LDLT, despite no difference in recipient age [75]. Donor age was an independent prognostic factor in LDLT. An experimental study in the mouse model showed an age-related loss of fenestration of LSECs together with thickening of the endothelium, basal lamina formation, and collagen deposition in the Space of Disse [76]. These age-related structural changes of LSECs and Space of Disse ultimately decrease sinusoidal perfusion. The impairment of regeneration in the aged liver is due, in part, to such a dysfunction of LSEC in addition to the reduction of sinusoidal blood flow. In addition, aged liver is associated with decreased intrahepatic energy source, ATP levels, caused by mitochondrial dysfunction [77]. In a recent study, mitochondrial dysfunction-associated senescence was reported [78]. Autophagy increases in accordance with the accumulation of damaged mitochondria and leads to cell death [79]. These mechanisms might be also partially related to impaired regeneration in aged livers.