Lipoproteins and Fibrinogen in Atherogenesis

1979 ◽  
Author(s):  
K.W. Walton

Previous work from this and other laboratories has shown that material antigenically related to the low-density lipoproteins (LDL) and to fibrinogen is demonstrable in atherosclerotic plaques. When arterial intima is extracted electrophoretically, ‘bound’ and ‘labile’ fractions of these antigens are in each case demonstrable. In the case of the “bound’ fraction of fibrinogen-related antigen (FRA) it has not been clear as to whether the material is in the form of native fibrinogen, as fibrin monomer, or as fibrin. To examine this problem fresh-frozen sections of arteries containing FRA have been examined by immunohistological techniques using antisera specific for fibrinogen, fibrinopeptides, plasmin and fibronectin. The results obtained with these antisera will be compared with one another and with results obtained with antisera to the antigens of LDL.

Inflammasome ◽  
2014 ◽  
Vol 1 (1) ◽  
Author(s):  
Maria Teresa Montero-Vega

AbstractLow-density lipoproteins become oxidised (ox-LDL) when retained in the arterial intima and are considered to be the inducers of inflammation in atherosclerosis. Peroxidation of phospholipids generates a variety of oxidised molecules in LDL and leads to the formation of oxidised lipid-protein adducts. These oxidative modifications are the target of various pattern recognition receptors (PRRs) and constitute immunogenic neoepitopes, termed oxidation-specific epitopes (OSEs). OSEs are thought to be a class of danger-associated molecular patterns (DAMPs) that mediate pro-inflammatory signals in atherosclerosis. Nevertheless, identical OSEs are generated on apoptotic cells that are identified by innate immunity through the same receptors to promote housekeeping tasks and immunosuppression. The present study provides an alternative point of view and proposes that OSEs are ‘waste-associated molecular patterns’ (WAMPs) recognised by innate immunity as a signal for the presence of oxidised waste that must be cleared without triggering inflammation. The hypothesis presented here states that ox-LDL are not inflammatory per se but instead polarise macrophages for housekeeping functions; however, other immune alerts, which are generated under the influence of risk factors, cooperate with them in switching macrophage polarisation towards dangerous phenotypes that complicate atheromas with different tendencies. This hypothesis of ‘immune cooperation’ explains why atheromas grow silently for decades and reveals atherosclerosis to be a dynamic disease that begins with the retention and oxidation of LDL in the arterial intima and ends with the formation of a thrombus, but in which the underlying immune process changes over time and differs between patients.


2021 ◽  
Vol 66 (3) ◽  
pp. 221
Author(s):  
V.I. Grytsay

A mathematical model of atherosclerosis of a blood vessel is advanced with regard for the entry of low-density lipoproteins (LDLs) into blood. For the first time, the influence of cytokines on the inflammation of a blood vessel at the formation of atherosclerotic plaques is taken into account. With the help of the expansion in a Fourier series and the calculation of an invariant measure, the scenario of the appearance of strange attractors depending on a change in the parameter of the dissipation of cholesterol is studied. The conclusion is made about the interconnection of the dynamics of the metabolic process in a blood vascular system and its physical state.


2021 ◽  
pp. 30-32
Author(s):  
A. V. Yagensky

The role of coronary heart disease and acute coronary syndrome in the structure of morbidity and mortality of the population of Ukraine cannot be overestimated. The main pathogenetic mechanism of corticosteroids is atherothrombosis, the influence of which is the basis of treatment of patients with coronary heart disease with or without corticosteroids. The effect on the progression of atherothrombosis is possible due to statins, due to slowing the growth of atherosclerotic plaques in blood vessels by reducing the level of low-density lipoproteins in the blood.


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