A new FGF1 variant protects against adriamycin-induced cardiotoxicity via modulating p53 activity

Xiao, Mengjie; Tang, Yufeng; Wang, Jie; Lu, Guangping; Niu, Jianlou; Li, Jiahao; Liu, Qingbo; Wang, Zhaoyun; Huang, Zhifeng; Guo, Yuanfang; Gao, Ting; Zhang, Xiaohui; Yue, Shouwei; Gu, Junlian

doi:10.1016/j.redox.2021.102219

Cited by 18 publications

(7 citation statements)

References 53 publications

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“…Upstream of SIRT1, in addition to miRNAs, a novel fibroblast growth factor 1 variant could counteract adriamycin-induced apoptosis by decreasing p53 activity via upregulation of SIRT1-mediated p53 deacetylation. 235 There have also been a series of studies on the antiapoptotic effect of melatonin which regulates SIRT1 in various physiological processes. [236][237][238][239] Additionally, some chemicals or drugs, like cambinol and ginsenoside Rc, have been shown to inhibit or activate SIRT1 to regulate the apoptotic process.…”

Section: The Regulatory Role Of Sirts In Cellular Biologymentioning

confidence: 99%

The sirtuin family in health and disease

Zhang

Chen

et al. 2022

Sig Transduct Target Ther

296

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Sirtuins (SIRTs) are nicotine adenine dinucleotide(+)-dependent histone deacetylases regulating critical signaling pathways in prokaryotes and eukaryotes, and are involved in numerous biological processes. Currently, seven mammalian homologs of yeast Sir2 named SIRT1 to SIRT7 have been identified. Increasing evidence has suggested the vital roles of seven members of the SIRT family in health and disease conditions. Notably, this protein family plays a variety of important roles in cellular biology such as inflammation, metabolism, oxidative stress, and apoptosis, etc., thus, it is considered a potential therapeutic target for different kinds of pathologies including cancer, cardiovascular disease, respiratory disease, and other conditions. Moreover, identification of SIRT modulators and exploring the functions of these different modulators have prompted increased efforts to discover new small molecules, which can modify SIRT activity. Furthermore, several randomized controlled trials have indicated that different interventions might affect the expression of SIRT protein in human samples, and supplementation of SIRT modulators might have diverse impact on physiological function in different participants. In this review, we introduce the history and structure of the SIRT protein family, discuss the molecular mechanisms and biological functions of seven members of the SIRT protein family, elaborate on the regulatory roles of SIRTs in human disease, summarize SIRT inhibitors and activators, and review related clinical studies.

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Section: The Regulatory Role Of Sirts In Cellular Biologymentioning

confidence: 99%

The sirtuin family in health and disease

Zhang

Chen

et al. 2022

Sig Transduct Target Ther

296

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“…Multiple works identified that fibroblast growth factor 1 (FGF1) is elevated by oxidative damage, implying that an increased FGF1 expression is an adaptive response and might be protective under different kinds of stresses. Our previous study revealed that FGF1 displayed therapeutics and favorable effects on maintaining myocardial redox homeostasis and improving cardiac function, especially in the setting of DOX treatment [ 8 , 9 ]. Beyond that, FGF1 is now emerging as possessing various protective effects including but not restricted to promoting angiogenesis [ 10 ] and alleviating apoptosis [ 11 ] and fibrosis [ 9 ] through partly attenuating oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

“…Our previous study revealed that FGF1 displayed therapeutics and favorable effects on maintaining myocardial redox homeostasis and improving cardiac function, especially in the setting of DOX treatment [ 8 , 9 ]. Beyond that, FGF1 is now emerging as possessing various protective effects including but not restricted to promoting angiogenesis [ 10 ] and alleviating apoptosis [ 11 ] and fibrosis [ 9 ] through partly attenuating oxidative stress. These findings support the idea that FGF1 has a great potency in the prevention and treatment of heart injury in response to stresses.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Liu

Gao

et al. 2022

Nutrients

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Doxorubicin (DOX) has received attention due to dose-dependent cardiotoxicity through abnormal redox cycling. Native fibroblast growth factor 1 (FGF1) is known for its anti-oxidative benefits in cardiovascular diseases, but possesses a potential tumorigenic risk. Coincidentally, the anti-proliferative properties of resveratrol (RES) have attracted attention as alternatives or auxiliary therapy when combined with other chemotherapeutic drugs. Therefore, the purpose of this study is to explore the therapeutic potential and underlying mechanisms of co-treatment of RES and FGF1 in a DOX-treated model. Here, various cancer cells were applied to determine whether RES could antagonize the oncogenesis effect of FGF1. In addition, C57BL/6J mice and H9c2 cells were used to testify the therapeutic potential of a co-treatment of RES and FGF1 against DOX-induced cardiotoxicity. We found RES could reduce the growth-promoting activity of FGF1. Additionally, the co-treatment of RES and FGF1 exhibits a more powerful cardio-antioxidative capacity in a DOX-treated model. The inhibition of SIRT1/NRF2 abolished RES in combination with FGF1 on cardioprotective action. Further mechanism analysis demonstrated that SIRT1 and NRF2 might form a positive feedback loop to perform the protective effect on DOX-induced cardiotoxicity. These favorable anti-oxidative activities and reduced proliferative properties of the co-treatment of RES and FGF1 provided a promising therapy for anthracycline cardiotoxicity during chemotherapy.

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“…Conditional cardiac-specific HUWE1 (a ubiquitin E3 ligase) knockout mice developed cardiac hypertrophy, accompanied by impaired mitochondrial energy metabolism and ROS defense [ 85 ]. The reversal of murine double minute 2 (MDM2), a p53-specific E3 ubiquitin ligase, and SIRT1 reduced the activity of the apoptosis factor p53 through SIRT1-mediated p53 deacetylation and MDM2-mediated p53 ubiquitination, which alleviated oxidative stress and cell apoptosis in the tissues and cells of a cardiomyopathy model induced by adriamycin [ 86 ].…”

Section: Interaction Of the Ups And Oxidative Stress In Cvdsmentioning

confidence: 99%

Intersection of the Ubiquitin–Proteasome System with Oxidative Stress in Cardiovascular Disease

Qiu

Chen²,

Li³

et al. 2022

IJMS

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Cardiovascular diseases (CVDs) present a major social problem worldwide due to their high incidence and mortality rate. Many pathophysiological mechanisms are involved in CVDs, and oxidative stress plays a vital mediating role in most of these mechanisms. The ubiquitin–proteasome system (UPS) is the main machinery responsible for degrading cytosolic proteins in the repair system, which interacts with the mechanisms regulating endoplasmic reticulum homeostasis. Recent evidence also points to the role of UPS dysfunction in the development of CVDs. The UPS has been associated with oxidative stress and regulates reduction–oxidation homeostasis. However, the mechanisms underlying UPS-mediated oxidative stress’s contribution to CVDs are unclear, especially the role of these interactions at different disease stages. This review highlights the recent research progress on the roles of the UPS and oxidative stress, individually and in combination, in CVDs, focusing on the pathophysiology of key CVDs, including atherosclerosis, ischemia–reperfusion injury, cardiomyopathy, and heart failure. This synthesis provides new insight for continued research on the UPS–oxidative stress interaction, in turn suggesting novel targets for the treatment and prevention of CVDs.

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A new FGF1 variant protects against adriamycin-induced cardiotoxicity via modulating p53 activity

Cited by 18 publications

References 53 publications

The sirtuin family in health and disease

The sirtuin family in health and disease

Resveratrol and FGF1 Synergistically Ameliorates Doxorubicin-Induced Cardiotoxicity via Activation of SIRT1-NRF2 Pathway

Intersection of the Ubiquitin–Proteasome System with Oxidative Stress in Cardiovascular Disease

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