Cholesterol homeostasis: Researching a dialogue between the brain and peripheral tissues

Gliozzi, Micaela; Musolino, Vincenzo; Bosco, Francesca; Scicchitano, Miriam; Scarano, Federica; Nucera, Saverio; Zito, Maria Caterina; Ruga, Stefano; Carresi, Cristina; Macrì, Roberta; Guarnieri, Lorenza; Maiuolo, Jessica; Tavernese, Annamaria; Coppoletta, Anna Rita; Nicita, Caterina; Mollace, Vincenzo; Muscoli, Carolina; Belzung, Catherine

doi:10.1016/j.phrs.2020.105215

Cited by 62 publications

(64 citation statements)

References 413 publications

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“…the plasticity of membranes [7]. This is especially important for mitochondria, which are considered the energy source of the cell, in which cholesterol is fundamental to membrane maintenance [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

“…Cholesterol in cells is essential for the correct organization of the cell membrane, determines its permeability and fluidity and is considered an important factor that regulates the plasticity of membranes [ 7 ]. This is especially important for mitochondria, which are considered the energy source of the cell, in which cholesterol is fundamental to membrane maintenance [ 8 , 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

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MitoQ Is Able to Modulate Apoptosis and Inflammation

Piscianz

Tesser

Rimondi

et al. 2021

IJMS

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Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of several neurodegenerative diseases. The present study aimed to examine the impact of the inflammation platform activation on the neuronal cell line (DAOY) treated with specific inflammatory stimuli and whether MitoQ addition can modulate these deregulations. DAOY cells were pre-treated with MitoQ and then stimulated by a blockade of the cholesterol pathway, also called mevalonate pathway, using a statin, mimicking cholesterol deregulation, a common parameter present in some neurodegenerative and autoinflammatory diseases. To verify the role played by MitoQ, we examined the expression of genes involved in the inflammation mechanism and the mitochondrial activity at different time points. In this experimental design, MitoQ showed a protective effect against the blockade of the mevalonate pathway in a short period (12 h) but did not persist for a long time (24 and 48 h). The results obtained highlight the anti-inflammatory properties of MitoQ and open the question about its application as an effective adjuvant for the treatment of the autoinflammatory disease characterized by a cholesterol deregulation pathway that involves mitochondrial homeostasis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MitoQ Is Able to Modulate Apoptosis and Inflammation

Piscianz

Tesser

Rimondi

et al. 2021

IJMS

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“…The occurrence of these events was studied in depth in an animal model of MAFLD resembling the human features of disease development 39 , con rming that chronic intake of a diet enriched in fats and carbohydrates contributes to induce in ammation and oxidative damage primarily to the hepatic microcirculation and then, at systemic level 40,41 . This suggests a more generalized endothelial dysfunction, also involving blood-brain barrier that, once damaged, permits the in ltration of circulating in ammatory cells into the brain 42 .…”

Section: Discussionmentioning

confidence: 94%

Mafld Causes Alterations in Thalamus Energy Metabolism and Brain Structure

Nucera

Ruga

Cardamone

et al. 2021

Preprint

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Background Metabolic associated fatty liver disease (MAFLD), commonly known as non-alcoholic fatty liver disease, represents a continuum of events characterized by excessive hepatic fat accumulation which can progress to nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and in some severe cases hepatocellular carcinoma. MAFLD might be considered as a multisystem disease that affects not only the liver but involves wider implications, relating to several organs and systems, the brain included. The present study aims to investigate changes associated with MAFLD-induced alteration of thalamic metabolism in vivo. Methods DIAMOND mice were fed a chow diet and tap water (NC NW) or fat Western Diet (WD SW) for up to 28 weeks. At the baseline and weeks 4, 8, 20, 28 the thalamic neurochemical profile and total cerebral brain volume were evaluated longitudinally in both diet groups using 1H-MRS. To confirm the disease progression, at each time point, a subgroup of animals was sacrificed, the livers excised and placed in formalin. Liver histology was assessed and reviewed by an expert liver pathologist. Results MAFLD development significantly increases the thalamic levels of total N-acetylaspartate, total creatine, total choline, and taurine. Furthermore, in the WD SW group a reduction in total cerebral brain volume has been observed (p < 0.05 vs NC NW). Conclusion Our results suggest that thalamic energy metabolism is affected by MAFLD progression. This metabolic imbalance, that is quantifiable by 1H-MRS in vivo, might cause structural damage to brain cells and dysfunctions of neurotransmitter release.

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“…In addition to contributing to the structural organization of the cell by providing building blocks that maintain membrane plasticity, lipids play dynamic roles in membrane trafficking and signal transduction ( Grouleff et al, 2015 ; Santos and Preta, 2018 ). By reason of its structural as well as functional relevance, lipid metabolism is a tightly regulated process that is influenced by the balance between endogenous or de novo synthesis of cholesterol and its exogenous or dietary intake in the body ( Gliozzi et al, 2021 ).…”

Section: Lipids: An Overviewmentioning

confidence: 99%

Pathological Crosstalk Between Oxidized LDL and ER Stress in Human Diseases: A Comprehensive Review

Varghese

Ali

2021

Front. Cell Dev. Biol.

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The oxidative modification of the major cholesterol carrying lipoprotein, oxLDL, is a biomarker as well as a pathological factor in cardiovascular diseases (CVD), type 2 diabetes mellitus (T2DM), obesity and other metabolic diseases. Perturbed cellular homeostasis due to physiological, pathological and pharmacological factors hinder the proper functioning of the endoplasmic reticulum (ER), which is the major hub for protein folding and processing, lipid biosynthesis and calcium storage, thereby leading to ER stress. The cellular response to ER stress is marked by a defensive mechanism called unfolded protein response (UPR), wherein the cell adapts strategies that favor survival. Under conditions of excessive ER stress, when the survival mechanisms fail to restore balance, UPR switches to apoptosis and eliminates the defective cells. ER stress is a major hallmark in metabolic syndromes such as diabetes, non-alcoholic fatty liver disease (NAFLD), neurological and cardiovascular diseases. Though the pathological link between oxLDL and ER stress in cardiovascular diseases is well-documented, its involvement in other diseases is still largely unexplored. This review provides a deep insight into the common mechanisms in the pathogenicity of diseases involving oxLDL and ER stress as key players. In addition, the potential therapeutic intervention of the targets implicated in the pathogenic processes are also explored.

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Cholesterol homeostasis: Researching a dialogue between the brain and peripheral tissues

Cited by 62 publications

References 413 publications

MitoQ Is Able to Modulate Apoptosis and Inflammation

MitoQ Is Able to Modulate Apoptosis and Inflammation

Mafld Causes Alterations in Thalamus Energy Metabolism and Brain Structure

Pathological Crosstalk Between Oxidized LDL and ER Stress in Human Diseases: A Comprehensive Review

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