A novel function for fibroblast growth factor 21: stimulation of NADPH oxidase-dependent ROS generation

Wang, Wenfei; Ma, Lei; Liu, Mingyao; Zhao, Tingting; Zhang, Tong; Yang, Yuexin; Cao, Hongxue; Han, Xiaohui; Li, Deshan

doi:10.1007/s12020-014-0502-9

Cited by 8 publications

(6 citation statements)

References 42 publications

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“…The finding that adipsin-deficiency resulted in a significant increase of the serum levels of FGF-21 and adiponectin is interesting as both adipokines were reported to have metabolic/anti-inflammatory effects and suggested to be instrumental in maintaining joint health [53][54][55][56][57]. FGF-21 is an adipokine/endocrine hormone produced by the liver, adipose tissue and blood cells [58,59], and is reported to be anti-inflammatory and to demonstrate antiaging properties [60,61]. Importantly and related to arthritis, FGF-21 was found to attenuate the collageninduced arthritis by reducing, among other things, some pro-inflammatory cytokines [55].…”

Section: Discussionmentioning

confidence: 99%

“…Although a relationship between the expression of adipsin and FGF-21 has been reported [62], the regulatory factors at play still remain to be determined. FGF-21 is known to be regulated by a number of metabolic factors, nutrients, and oxidative stress [58,63,64], and involved in the regulation of glucose and lipid metabolism [65][66][67][68]. This could suggest that the lack of adipsin impacted these metabolic factors.…”

Section: Discussionmentioning

confidence: 99%

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In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice

Paré

Tardif

Fahmi

et al. 2020

Aging

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The adipokine adipsin is an emerging mediator of human osteoarthritis (OA) progression. Here, we investigated its in vivo role in the development of spontaneous OA in aging mice. We compared articular knee joint morphology, histology in knee cartilage, synovial membrane, subchondral bone, meniscus, and anterior cruciate ligament (ACL), and chondrogenesis in the ACL from adipsin-deficient (Df-/-) and wild-type (Df +/+) in 20-week-and 20-month-old mice. Serum levels of a panel of adipokines, inflammatory factors, and metalloproteases known to be implicated in OA were investigated. Data first reveal that the early manifestation of OA appeared in the ACL of 20-week-old mice, progressing to severe alterations in the 20 month-old wild-type mice. Further results demonstrated that adipsin-deficiency protected the articular tissues from spontaneous OA progression and triggered significantly higher serum levels of the adipokines adiponectin and FGF-21 while lowering levels of the inflammatory factor interleukin 6 (IL-6) in both young and old mice. This work further underlines the clinical relevance of adipsin as a novel therapeutic approach of human OA. Moreover, this study shows the potential beneficial effect of the adipokine FGF-21 against OA, and provides support for this factor to be a new biomarker and/or target of primary OA therapeutic avenues.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice

Paré

Tardif

Fahmi

et al. 2020

Aging

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“…The same study found no effect of MMP9 genetic depletion on oxygen-induced retinopathy. PEDF promotes metabolism of oxygen radicals by stimulating glutamine synthetase and l-glutamate/l-glutamate transporter levels in neonatal mice with oxygen-induced retinopathy ( 96 ). Modifying PEDF levels through intravitreal drug injections has been investigated as a possible approach to prevent ROP.…”

Section: Pigment Epithelium Derived Factormentioning

confidence: 99%

A Pathogenic Relationship of Bronchopulmonary Dysplasia and Retinopathy of Prematurity? A Review of Angiogenic Mediators in Both Diseases

et al. 2018

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Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are common and significant morbidities of prematurely born infants. These diseases have in common altered and pathologic vascular formation in the face of incomplete organ development. Therefore, it is reasonable to question whether factors affecting angiogenesis could have a joint pathogenic role for both diseases. Inhibition or induced expression of a single angiogenic factor is unlikely to be 100% causative or protective of either of BPD or ROP. It is more likely that interactions of multiple factors leading to disordered angiogenesis are present, increasing the likelihood of common pathways in both diseases. This review explores this possibility by assessing the evidence showing involvement of specific angiogenic factors in the vascular development and maldevelopment in each disease. Theoretical interactions of specific factors mutually contributing to BPD and ROP are proposed and, where possible, a timeline of the proposed relationships between BPD and ROP is developed. It is hoped that future research will be inspired by the theories put forth in this review to enhance the understanding of the pathogenesis in both diseases.

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“…Among peripheral blood leukocytes, FGF21 was highly expressed in monocytes and neutrophils ( 81 ). By increasing the expression of GLUT-1, FGF21 upregulated the ability to uptake glucose in activated monocytes, which can be beneficial in immune activation ( 82 ).…”

Section: Fgf21 In Inflammationmentioning

confidence: 99%

Mechanism of fibroblast growth factor 21 in cardiac remodeling

Zhao

Cui

Liao

2023

Front. Cardiovasc. Med.

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Cardiac remodeling is a basic pathological process that enables the progression of multiple cardiac diseases to heart failure. Fibroblast growth factor 21 is considered a regulator in maintaining energy homeostasis and shows a positive role in preventing damage caused by cardiac diseases. This review mainly summarizes the effects and related mechanisms of fibroblast growth factor 21 on pathological processes associated with cardiac remodeling, based on a variety of cells of myocardial tissue. The possibility of Fibroblast growth factor 21 as a promising treatment for the cardiac remodeling process will also be discussed.

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A novel function for fibroblast growth factor 21: stimulation of NADPH oxidase-dependent ROS generation

Cited by 8 publications

References 42 publications

In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice

In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice

A Pathogenic Relationship of Bronchopulmonary Dysplasia and Retinopathy of Prematurity? A Review of Angiogenic Mediators in Both Diseases

Mechanism of fibroblast growth factor 21 in cardiac remodeling

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