Metabolic syndrome and nonalcoholic fatty liver disease. The role of endothelial progenitor cells♦

Gutiérrez-Grobe, Ylse; Gavilanes-Espinar, Juan G; Massó-Rojas, Felipe; Sánchez-Valle, Vicente; Páez, Araceli; Ponciano-Rodríguez, Guadalupe; Chávez-Tapia, Norberto C.; Uribe, Misael; Méndez-Sánchez, Nahúm

doi:10.1016/s1665-2681(19)31296-7

Cited by 9 publications

(4 citation statements)

References 22 publications

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“…However, it has been shown that the number of EPCs was higher in patients with NAFLD and MetS in comparison to those without these conditions, and that the EPCs number was directly proportional to the degree of liver steatosis. The increase in EPCs number could be considered as a compensatory mechanism against endothelial injury [100].…”

Section: Endothelial Progenitor Cells Dysfunction and Nafldmentioning

confidence: 99%

Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches

Peyter

Armengaud

Guillot

et al. 2021

IJMS

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Metabolic syndrome (MetS) is a cluster of several disorders, such as hypertension, central obesity, dyslipidemia, hyperglycemia, insulin resistance and non-alcoholic fatty liver disease. Despite health policies based on the promotion of physical exercise, the reduction of calorie intake and the consumption of healthy food, there is still a global rise in the incidence and prevalence of MetS in the world. This phenomenon can partly be explained by the fact that adverse events in the perinatal period can increase the susceptibility to develop cardiometabolic diseases in adulthood. Individuals born after intrauterine growth restriction (IUGR) are particularly at risk of developing cardiovascular diseases (CVD) and metabolic disorders later in life. It has been shown that alterations in the structural and functional integrity of the endothelium can lead to the development of cardiometabolic diseases. The endothelial progenitor cells (EPCs) are circulating components of the endothelium playing a major role in vascular homeostasis. An association has been found between the maintenance of endothelial structure and function by EPCs and their ability to differentiate and repair damaged endothelial tissue. In this narrative review, we explore the alterations of EPCs observed in individuals with cardiometabolic disorders, describe some mechanisms related to such dysfunction and propose some therapeutical approaches to reverse the EPCs dysfunction.

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Section: Endothelial Progenitor Cells Dysfunction and Nafldmentioning

confidence: 99%

Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches

Peyter

Armengaud

Guillot

et al. 2021

IJMS

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“…According to recent manuscript, these cells may play a role in the early natural history of NAFLD. EPC might be increased in an attempt to repair the endothelial damage resulting from metabolic alterations accompanying NAFLD[83]. …”

Section: Pathophysiological Mechanisms Linking Nafld and Cvdmentioning

confidence: 99%

Nonalcoholic fatty liver disease - A multisystem disease?

Mikolašević

Milić

Wensveen

et al. 2016

WJG

154

155

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common comorbidities associated with overweight and metabolic syndrome (MetS). Importantly, NAFLD is one of its most dangerous complications because it can lead to severe liver pathologies, including fibrosis, cirrhosis and hepatic cellular carcinoma. Given the increasing worldwide prevalence of obesity, NAFLD has become the most common cause of chronic liver disease and therefore is a major global health problem. Currently, NAFLD is predominantly regarded as a hepatic manifestation of MetS. However, accumulating evidence indicates that the effects of NAFLD extend beyond the liver and are negatively associated with a range of chronic diseases, most notably cardiovascular disease (CVD), diabetes mellitus type 2 (T2DM) and chronic kidney disease (CKD). It is becoming increasingly clear that these diseases are the result of the same underlying pathophysiological processes associated with MetS, such as insulin resistance, chronic systemic inflammation and dyslipidemia. As a result, they have been shown to be independent reciprocal risk factors. In addition, recent data have shown that NAFLD actively contributes to aggravation of the pathophysiology of CVD, T2DM, and CKD, as well as several other pathologies. Thus, NAFLD is a direct cause of many chronic diseases associated with MetS, and better detection and treatment of fatty liver disease is therefore urgently needed. As non-invasive screening methods for liver disease become increasingly available, detection and treatment of NAFLD in patients with MetS should therefore be considered by both (sub-) specialists and primary care physicians.

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“…Importantly, the transplanted EPCs were not differentiated into either hepatocytes or endothelial cells, confirming that the BM-EPCs exert these beneficial effects, most likely by acting on surrounding cells rather than their direct interaction [ 93 , 100 ]. An increased number of BM-EPCs in NAFLD patients was considered to be a compensatory mechanism against the endothelial injury observed during NAFLD progression, and it was proportionally associated with the degree of liver steatosis [ 96 , 101 ]. On the contrary, a reduced number and function of circulating BM-EPCs in patients with NAFLD was reported by Chiang et al This study revealed that the circulating BM-EPC population can be used as an independent reverse predictor of NAFLD [ 102 ].…”

Section: Endothelial Cells In the Pathogenesis Of Nafldmentioning

confidence: 99%

Endothelial Cell Dysfunction and Nonalcoholic Fatty Liver Disease (NAFLD): A Concise Review

Nasiri-Ansari

Ανδρουτσάκος

Flessa

et al. 2022

Cells

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Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide. It is strongly associated with obesity, type 2 diabetes (T2DM), and other metabolic syndrome features. Reflecting the underlying pathogenesis and the cardiometabolic disorders associated with NAFLD, the term metabolic (dysfunction)-associated fatty liver disease (MAFLD) has recently been proposed. Indeed, over the past few years, growing evidence supports a strong correlation between NAFLD and increased cardiovascular disease (CVD) risk, independent of the presence of diabetes, hypertension, and obesity. This implies that NAFLD may also be directly involved in the pathogenesis of CVD. Notably, liver sinusoidal endothelial cell (LSEC) dysfunction appears to be implicated in the progression of NAFLD via numerous mechanisms, including the regulation of the inflammatory process, hepatic stellate activation, augmented vascular resistance, and the distortion of microcirculation, resulting in the progression of NAFLD. Vice versa, the liver secretes inflammatory molecules that are considered pro-atherogenic and may contribute to vascular endothelial dysfunction, resulting in atherosclerosis and CVD. In this review, we provide current evidence supporting the role of endothelial cell dysfunction in the pathogenesis of NAFLD and NAFLD-associated atherosclerosis. Endothelial cells could thus represent a “golden target” for the development of new treatment strategies for NAFLD and its comorbid CVD.

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Metabolic syndrome and nonalcoholic fatty liver disease. The role of endothelial progenitor cells♦

Cited by 9 publications

References 22 publications

Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches

Endothelial Progenitor Cells Dysfunctions and Cardiometabolic Disorders: From Mechanisms to Therapeutic Approaches

Nonalcoholic fatty liver disease - A multisystem disease?

Endothelial Cell Dysfunction and Nonalcoholic Fatty Liver Disease (NAFLD): A Concise Review

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