Statins are widely used in the management or inhibition of several processes that lead to the development of cardiovascular diseases. Increased statin therapy has been related to the induction of type II diabetes (DM), a state which predisposes to cardiovascular disease (CVD). Statins are well-known to possess anti-inflammatory properties and the ability to disrupt de novo biosynthesis of cholesterol and lipid homeostasis has been implicated in the induction of inflammatory responses within pancreatic β-cells. Inhibition of β-hydroxy β-methyl glutaryl-CoA (HMG-CoA) results an increased level of low-density lipoproteins (LDL) receptors. Increased LDL receptor numbers will replenish exhausted intracellular supplies, resulting in higher levels of intracellular cholesterol. Therefore, stimulating immunological response and inflammatory reactions, disrupt the functional integrity of the β-cell via oxidation of the plasma-derived low-density lipoprotein. Despite the pleiotropic effects of statins on the pancreatic β-cell, they have also been reported to affect a number of other cell types associated with the development of diabetes. Inhibition of the biosynthesis of isoprenoid by statins has been associated with the down-stream regulation of glucose transporter (GLUT 4) in adipose tissues, which facilitates the uptake of glucose. This effect resulted in increasing resistance to insulin in the liver, muscle, and adipose tissue. Adiponectin, a plasma protein released by adipocytes, alters fatty acids and carbohydrate metabolism both in the muscle cells and liver. This process indirectly influences resistance to insulin by the attendant decrease in hepatic gluconeogenesis and to upregulate muscular β-oxidation and glucose uptake.
Equilibrium between cell survival and death is important for normal cell homeostasis and development and also for inhibiting pathologies particularly cancer. Anastasis is a natural cell recovery phenomenon that rescues cells from the brink of death or a mechanism by which cells recuperate from apoptotic lesions and return to its normal active and functioning state. Programmed cell death (apoptosis) was known to be an intrinsically irreversible cascade that commits cells to a rapid destruction. However, recent studies have demonstrated the possibility of recovering dying cells even at the late stages. Anastasis uses the usual pro-metastatic and pro-survival factors to inhibit apoptotic progression. Epithelial mesenchymal transition (EMT) activation and its related modulators is not only linked with cellular metastasis and survivability but also widely associated with the stemness of cancer cells.
Mitochondrial dysfunctions remained a pivotal mechanism in manifold neurodegenerative diseases. Mitochondrial homeostasis within the cell is an essential aspect of cell biology. Mitochondria which is also known as the power-generating set of the cell, have a dominant role in several processes associated with the genomic integrity and cellular equilibrium maintenance. They are involved in maintaining optimal cells functioning and guidance from possible DNA damage which could lead to mutations and onset of diseases. Conversely, system perturbations which could be due to environmental factors or senescence induce changes in the physiological balance and result in the mitochondrial functions impairment. The focal point of this review focuses on mitochondrial dysfunction as a significant condition in the onset of neuronal disintegration. We explain the pathways associated with the dysfunction of the mitochondria which are common amongst the most recurring neurodegenerative diseases including Alzheimers and Parkinsons disease. Do mitochondrial dysfunctions represent an early event in causing a shift towards neuropathological processes?
The impact of COVID-19 is significant in the body system, one of which is the central nervous system (CNS) involved in controlling all aspects of human behavior and coordination. This shows the need to assess from various studies in human and animal models the neurological effects of this virus. Some of the reported effects include loss of taste and smell, headaches, delirium, dizziness, ischemic stroke, and brain inflammation. It is essential to review the acute, chronic or transient neurological effects. This will enhance and/or improve treatment designs and management modalities for the COVID-19. We critically revise the literature and contribute to the body of knowledge in this line of research. Here in this chapter, we highlighted the various neurological disorders caused by COVID-19 and examined the relationship between the neurological systems and COVID-19. As well as evaluate current treatment/management modalities including vaccines and prospects for the future.
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