2016
DOI: 10.1002/jhbp.333
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Enhancing hepatic fibrosis in spontaneously hypertensive rats fed a choline‐deficient diet: a follow‐up report on long‐term effects of oxidative stress in non‐alcoholic fatty liver disease

Abstract: Hypertension precipitated hepatic steatosis, and further, acts as an enhancer in NAFLD progression to liver fibrosis through oxidative stress.

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Cited by 13 publications
(9 citation statements)
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“…Remarkably, ROS can interact directly with HSCs, which are the main executors of fibrogenesis to generate ECM. The cellular redox environment could regulate the entry of quiescent HSCs into activated cycle [24, 84]. Redox-sensitive transcription factors such as NF- κ B are important to regulate the activities of antioxidant enzymes that mediate ROS signaling.…”
Section: The Relationship and Interdependence Between Oxidative Stmentioning
confidence: 99%
“…Remarkably, ROS can interact directly with HSCs, which are the main executors of fibrogenesis to generate ECM. The cellular redox environment could regulate the entry of quiescent HSCs into activated cycle [24, 84]. Redox-sensitive transcription factors such as NF- κ B are important to regulate the activities of antioxidant enzymes that mediate ROS signaling.…”
Section: The Relationship and Interdependence Between Oxidative Stmentioning
confidence: 99%
“…Furthermore, NADPH oxidase NOX-generated ROS has been suggested to play a preeminent role in the pathogenesis of liver fibrosis by promoting myofibroblast activation [40]. Regardless of etiology, these ROS can directly activate the prime executors of fibrogenesis i-e, hepatic stellate cells (HSCs) to transform into myofibroblasts and produce ECM proteins and further enhance the cellular oxidative stress and inflammation [3,41]. Reflexively, this redox-sensitive cascade results in the onset and exasperation of redox-related progression of liver fibrosis [7,35].…”
Section: Oxidative Stress Mediated Biomarkersmentioning
confidence: 99%
“…Several studies have shown a relationship between hypertension and NAFLD from the viewpoint of prevalence, natural course, and effects of antihypertensive agents [3][4][5][6][7]. Our previous studies reported that a reduction in antioxidant capacity played a critical role in the development of both steatosis and fibrosis in a hypertensive NAFLD model [8,9].…”
Section: Introductionmentioning
confidence: 96%
“…Systolic blood pressure (BP) and diastolic BP in 7‐week‐old SHR have been reported to be 161 ± 5 and 133 ± 5 mmHg, respectively . We previously described a hypertensive NAFLD model without obesity and DM by feeding SHRs a choline‐deficient (CD) diet for 5 weeks .…”
Section: Introductionmentioning
confidence: 99%