Fibroblast Growth Factor 10 Attenuates Renal Damage by Regulating Endoplasmic Reticulum Stress After Ischemia–Reperfusion Injury

Tan, Xiaohua; Liu, Yu; Yang, Ruo; Tao, Qianyu; Xiang, Liangzhong; Xiao, Jian; Zhang, Jin‐San

doi:10.3389/fphar.2020.00039

Cited by 19 publications

(18 citation statements)

References 62 publications

(74 reference statements)

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“…Activation of PI3K pathway has been reported to underlie FGF10-mediated protection against I/R-induced endothelial cell apoptosis and barrier dysfunction (Fang et al, 2014). More recent studies provided further evidence that exogenous recombinant FGF10 mediates protection against renal IRI through suppression of excessive autophagy and ER stress (Tan et al, 2018;Tan et al, 2020), which will be further discussed later.…”

Section: Exogenous Fgf10 Protects Against Irimentioning

confidence: 85%

“…FGF10 effectively alleviated IRI evoked expression of ER stress-related proteins in the kidney including CHOP, GRP78, XBP-1, and ATF-4 and ATF-6, which may contribute to inhibit IR-induced activation of proapoptotic caspase-3 and Bax expression. Results from IRI model in vivo and in vitro cell culture experiments together indicate that FGF10 attenuates renal tubular epithelial cell death via inhibiting excessive ER stress, which is, at least in part, mediated by MEK-ERK1/2 signaling pathway (Tan et al, 2020). Therefore, FGF10 contributes to restore the balance between the adaptive pathway and the apoptotic pathway of UPR by inhibiting excessive ER stress.…”

Section: Fgf10 Inhibits Excessive Autophagy and Er Stressmentioning

confidence: 97%

“…A large amount of calcium ion influx results in ROS activation, which also leads to increase in TGF-b expression and its down stream signalling to promote fibrosis. (Cuevas et al, 1999); Antiapoptosis and regeneration (Fu et al, 2004;Weng et al, 2004) FGF2 Paracrine Attenuating mitochondrial damage and proinflammatory response (Tan et al, 2017) reduce renal damage and participate in the regeneration (Villanueva et al, 2006) FGF7 FGF7 Paracrine Promote bladder progenitor proliferation (Vinsonneau et al, 2010) FGF10 Paracrine Antiapoptosis and inflammatory response; suppressing excessive autophagy and ER stress (Tan et al, 2018;Tan et al, 2020) FGF19…”

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confidence: 99%

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Fibroblast Growth Factors in the Management of Acute Kidney Injury Following Ischemia-Reperfusion

et al. 2020

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Ischemia-reperfusion injury (IRI), which is triggered by a transient reduction or cessation of blood flow followed by reperfusion, is a significant cause of acute kidney injury (AKI). IRI can lead to acute cell death, tissue injury, and even permanent organ dysfunction. In the clinic, IRI contributes to a higher morbidity and mortality and is associated with an unfavorable prognosis in AKI patients. Unfortunately, effective clinical drugs to protect patients against the imminent risk of renal IRI or treat already existing AKI are still lacking. Fibroblast growth factors (FGFs) are important regulators of key biological and pathological processes, such as embryonic development, metabolic homeostasis and tumorigenesis through the regulation of cell differentiation, migration, proliferation and survival. Accumulating evidence suggests that altered expression of endogenous FGFs is associated with IRI and could be instrumental in mediating the repair process. Therefore, FGFs have been proposed as potential biomarkers in the clinic. More importantly, exogenous FGF ligands have been reported to protect against renal IRI and display promising features for therapy. In this review, we summarize the evidence and mechanisms of AKI following IRI with a focus on the therapeutic capacity of several members of the FGF family to treat AKI after IRI.

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Section: Exogenous Fgf10 Protects Against Irimentioning

confidence: 85%

Section: Fgf10 Inhibits Excessive Autophagy and Er Stressmentioning

confidence: 97%

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confidence: 99%

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Fibroblast Growth Factors in the Management of Acute Kidney Injury Following Ischemia-Reperfusion

et al. 2020

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“…All graphical data are the means ± SD from three independent experiments, "#" and "##" indicate significantly different from the untreated control group at the p < 0.05 and p < 0.01 levels, respectively, "*" and "**" indicate significantly different from the UVB only control group at the p < 0.05 and p < 0.01 levels, respectively. 2018; Dong et al, 2019;Tan et al, 2020). Previous studies have focused on the role of KGF-2 in embryonic development, wound healing, and tissue regeneration.…”

Section: Discussionmentioning

confidence: 99%

Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway

et al. 2021

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Objective: Exposure to ultraviolet B (UVB) can cause skin damage through oxidative stress, DNA damage, and apoptosis. Keratinocyte growth factor (KGF) has been shown to reduce the content of intracellular reactive oxygen species (ROS) following UVB exposure, a role that is crucial for the efficient photoprotection of skin. The present study evaluated the photoprotective effect of KGF-2 on UVB-induced skin damage and explored its potential molecular mechanism.Methods: To evaluate the effect of KGF-2 on UVB-induced damage ex vivo, a human epidermal full-thickness skin equivalent was pretreated without or with KGF-2 and then exposed to UVB and the levels of histopathological changes, DNA damage, inflammation, and apoptosis were then evaluated. The ability of KGF-2 to protect the cells against UVB-inflicted damage and its effect on ROS production, apoptosis, and mitochondrial dysfunction were determined in HaCaT cells.Results: Pretreatment of the epidermis with KGF-2 ameliorated the extent of photodamage. At the cellular level, KGF-2 could attenuate ROS production, apoptosis, DNA damage, and mitochondrial dysfunction caused by UVB exposure. KGF-2 could also activate the aryl hydrocarbon receptor (AhR) to trigger the Nrf2 signaling pathway.Conclusion: Taken together, our findings suggested that KGF-2 could ameliorate UVB-induced skin damage through inhibiting apoptosis, reducing oxidative stress, and preventing DNA damage and mitochondrial dysfunction via regulating AhR/Nrf2 signaling pathway.

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“…FGFs are potent angiogenic inducers 93 and seem to modulate ER stress and UPR. FGF1 treatment suppressed diabetes‐induced ER stress in an experimental model of diabetic nephropathy, 119 and FGF10 significantly attenuates the apoptosis of kidney tissues in AKI caused by renal ischaemia‐reperfusion injury by attenuating UPR 120 …”

Section: Vascular Growth Factors and Endoplasmic Reticulum Stress In mentioning

confidence: 97%

The endoplasmic reticulum stress and the unfolded protein response in kidney disease: Implications for vascular growth factors

Ricciardi

Gnudi

2020

J Cellular Molecular Medi

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Acute kidney injury (AKI) and chronic kidney disease (CKD) represent an important challenge for healthcare providers. The identification of new biomarkers/pharmacological targets for kidney disease is required for the development of more effective therapies. Several studies have shown the importance of the endoplasmic reticulum (ER) stress in the pathophysiology of AKI and CKD. ER is a cellular organelle devolved to protein biosynthesis and maturation, and cellular detoxification processes which are activated in response to an insult. This review aimed to dissect the cellular response to ER stress which manifests with activation of the unfolded protein response (UPR) with its major branches, namely PERK, IRE1α, ATF6 and the interplay between ER and mitochondria in the pathophysiology of kidney disease. Further, we will discuss the relationship between mediators of renal injury (with specific focus on vascular growth factors) and ER stress and UPR in the pathophysiology of both AKI and CKD with the aim to propose potential new targets for treatment for kidney disease.

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Fibroblast Growth Factor 10 Attenuates Renal Damage by Regulating Endoplasmic Reticulum Stress After Ischemia–Reperfusion Injury

Cited by 19 publications

References 62 publications

Fibroblast Growth Factors in the Management of Acute Kidney Injury Following Ischemia-Reperfusion

Fibroblast Growth Factors in the Management of Acute Kidney Injury Following Ischemia-Reperfusion

Keratinocyte Growth Factor 2 Ameliorates UVB-Induced Skin Damage via Activating the AhR/Nrf2 Signaling Pathway

The endoplasmic reticulum stress and the unfolded protein response in kidney disease: Implications for vascular growth factors

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