Study of Cellular Senescence and Vitamin D Deficiency in Nonalcoholic Fatty Liver Disease and The Potential Protective Effect of Vitamin D Supplementation

Al-ghamdi, Hasen A.; Fayez, Fayza F. Al; Bima, Abdulhadi; Khawaji, Taghreed M.; Elsamanoudy, Ayman Z.

doi:10.1016/j.jceh.2020.07.003

Cited by 7 publications

(6 citation statements)

References 50 publications

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“…Other experimental results from animal models of NAFLD induced by HFD, demonstrated that vitamin D deficiency was associated with increased cellular senescence and vitamin D supplementation normalized biochemical parameters. Vitamin D supplementation correlated with increased level of SMP-30, a senescence biomarker that is usually downregulated in NAFLD [180]. These results imply that the beneficial antioxidant effects of vitamin D are associated with its potential as a senescence modulator and might be useful in the treatment of NAFLD.…”

Section: Targeting Oxidative Stress To Modulate Cellular Senescencementioning

confidence: 74%

Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease

et al. 2022

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Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an important response to injury in the liver. Recent findings show that chronic oxidative stress can induce senescence, and this might be a driving mechanism for NAFLD progression, aggravating the disturbance of lipid metabolism, organelle dysfunction, pro-inflammatory response and hepatocellular damage. In this context, the modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression. This review focuses on the role of oxidative stress and senescence in the mechanisms leading to NAFLD and discusses the possibilities to modulate senescence as a therapeutic strategy in the treatment of NAFLD.

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Section: Targeting Oxidative Stress To Modulate Cellular Senescencementioning

confidence: 74%

Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease

et al. 2022

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“…Hepatic histological improvement with vitamin D3 replacement was also noted [132]. Additionally, vitamin D-treated rats showed overexpression of senescence marker protein 30 (SMP30), which is inversely related to NAFLD progression [126].…”

Section: The Association Between Nafld and Vddmentioning

confidence: 87%

“…The term NAFLD encompasses a range of hepatic disorders that occur with concomitant cardiometabolic disturbances, such as obesity and IR [125], and it reflects the hepatic manifestation of metabolic syndrome [126]. The hallmark of NAFLD is excessive fat accumulation within the liver (>5%) without considerable alcohol intake or any secondary causes of hepatic steatosis [125].…”

Section: Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

The Interplay of Vitamin D Deficiency and Cellular Senescence in The Pathogenesis of Obesity-Related Co-Morbidities

et al. 2021

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This scoping review aims to clarify the interplay between obesity, vitamin D deficiency, cellular senescence, and obesity-related metabolic consequences, mainly subclinical atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). Obesity is a significant global health problem that involves cellular, environmental, behavioral, and genetic elements. The fundamental cause of obesity throughout all life stages is an energy imbalance, and its consequences are countless and, foremost, very common. Obesity has been comprehensively studied in the literature given its association with low serum vitamin D, with many proposed mechanisms linking the two conditions. Moreover, markers of exaggerated cellular senescence have been proven to accumulate in obese individuals. Subclinical atherosclerosis initiates an early stage that ends in serious cardiac events, and obesity, low vitamin D, and senescent cells largely contribute to its associated chronic low-grade inflammation. Furthermore, NAFLD signifies the hepatic manifestation of metabolic syndrome, and studies have highlighted the important role of obesity, vitamin D deficiency, and cellular senescence in its development. Therefore, we outlined the most important mechanisms tying these conditions to one another.

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“…Some markers support senescence in the liver with NAFLD, and this includes p53, p21, p16, and, more specifically, senescence marker protein-30 (SMP30) [124][125][126]. SMP30 is involved in ROS and glucose breakdown and maintains calcium balance, but levels of SMP30 reduce with age [127]. Studies have shown that SMP30 reduces further in NAFLD [127].…”

Section: Mitochondrial Senescencementioning

confidence: 99%

“…SMP30 is involved in ROS and glucose breakdown and maintains calcium balance, but levels of SMP30 reduce with age [ 127 ]. Studies have shown that SMP30 reduces further in NAFLD [ 127 ]. A decrease in the amount of SMP30 causes fat accumulation in the liver and eventual death of hepatocytes due to the disruption of its metabolism [ 128 ].…”

Section: Reviewmentioning

confidence: 99%

Factors That Predict the Progression of Non-alcoholic Fatty Liver Disease (NAFLD)

Parameswaran¹,

Hasan²,

Sadeque³

et al. 2021

Cureus

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Non-alcoholic fatty liver disease (NAFLD) refers to a spectrum of diseases involving the deposition of fat in the hepatocytes of people with little to no alcohol consumption. NAFLD is associated with hypertension, diabetes, obesity, etc. As their prevalence increases, the propensity and severity of NAFLD might increase. As per the recently developed multi-hit hypothesis, factors like oxidative stress, genetic predisposition, lipotoxicity, and insulin resistance have been found to play a key role in the development of NAFLD and its associated complications. This article focuses on NAFLD, its pathophysiology, risk factors, and the various genetic and epigenetic factors involved in its development along with possible treatment modalities.We conducted an all-language literature search on Medline, Cochrane, Embase, and Google Scholar until October 2021. The following search strings and Medical Subject Heading (MeSH) terms were used: "NAFLD," "NASH," "Fibrosis," and "Insulin Resistance." We explored the literature on NAFLD for its epidemiology, pathophysiology, the role of various genes, and how they influence the disease and associated complications about the disease and its hepatic and extrahepatic complications. With its rapidly increasing prevalence rates across the world and serious complications like NASH and hepatocellular carcinoma, NAFLD is becoming a major public health issue and more research is needed to formulate better screening tools and treatment protocols.

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Study of Cellular Senescence and Vitamin D Deficiency in Nonalcoholic Fatty Liver Disease and The Potential Protective Effect of Vitamin D Supplementation

Cited by 7 publications

References 50 publications

Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease

Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease

The Interplay of Vitamin D Deficiency and Cellular Senescence in The Pathogenesis of Obesity-Related Co-Morbidities

Factors That Predict the Progression of Non-alcoholic Fatty Liver Disease (NAFLD)

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