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Article ; Online: A Review of Capacity Decay Studies of All-vanadium Redox Flow Batteries: Mechanism and State Estimation.

Wang, Yupeng / Mu, Anle / Wang, Wuyang / Yang, Bin / Wang, Jiahui

ChemSusChem

2024 , Page(s) e202301787

Abstract: As a promising large-scale energy storage technology, all-vanadium redox flow battery has garnered considerable attention. However, the issue of capacity decay significantly hinders its further development, and thus the problem remains to be ... ...

Abstract	As a promising large-scale energy storage technology, all-vanadium redox flow battery has garnered considerable attention. However, the issue of capacity decay significantly hinders its further development, and thus the problem remains to be systematically sorted out and further explored. This review provides comprehensive insights into the multiple factors contributing to capacity decay, encompassing vanadium cross-over, self-discharge reactions, water molecules migration, gas evolution reactions, and vanadium precipitation. Subsequently, it analyzes the impact of various battery parameters on capacity. Based on this foundation, the article expounds upon the significance of battery internal state estimation technology. Additionally, the review also summarizes domestic and international mathematical models utilized for simulating capacity decay, serving as a valuable reference for future research endeavors. Finally, through the comparison of traditional experimental methods and mathematical modeling methods, this article offers effective guidance for the future development direction of battery state monitoring. This review generally overview the problems related to the capacity attenuation of all-vanadium flow batteries, which is of great significance for understanding the mechanism behind capacity decay and state monitoring technology of all-vanadium redox flow battery.
Language	English
Publishing date	2024-03-05
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	1864-564X
ISSN (online)	1864-564X
DOI	10.1002/cssc.202301787
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Article: Low-Temperature Sintering of Bi(Ni

Wang, Wuyang / Wang, Shihao / Sun, Jun / Wang, Qiushi / Fang, Bijun

Materials (Basel, Switzerland)

2023 Volume 16, Issue 9

Abstract: A low-temperature sintering strategy was realized for preparing 0.21Bi( ... ...

Abstract	A low-temperature sintering strategy was realized for preparing 0.21Bi(Ni
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2487261-1
ISSN	1996-1944
ISSN	1996-1944
DOI	10.3390/ma16093459
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Article ; Online: Mulberry leaves attenuate D-galactose-induced aging in vivo and in vitro.

Zhu, Yan / Han, Yaping / Wang, Wuyang / Liang, Guangming / Qi, Jin

Journal of ethnopharmacology

2023 Volume 311, Page(s) 116286

Abstract: Ethnopharmacological relevance: Mulberry leaves contain many bioactive compounds and have been widely used in traditional medicines and functional foods for prevention and treatment of age-related diseases, such as diabetes, cognitive impairment and ... ...

Abstract	Ethnopharmacological relevance: Mulberry leaves contain many bioactive compounds and have been widely used in traditional medicines and functional foods for prevention and treatment of age-related diseases, such as diabetes, cognitive impairment and obesity-mediated liver cancer. Aging has an irreversible negative impact on human health for many years, even decades, before death, which is a social and economic burden on society. Aim of the study: The objective of this study was to investigate the antioxidant and anti-aging effects of mulberry leaf extract (MLE) in vivo and in vitro. Materials and methods: The Caenorhabditis elegans (C. elegans) was used as a model organism to observe the effects of different concentrations of MLE (1, 2, 4, 8 mg/mL) on nematodes' healthy lifespan, reproductive capacity, locomotion, stress resistance, and antioxidation. In addition, D-galactose (D-gal) induced liver aging in mice and L-02 cells were established. The antioxidant and anti-aging effects of MLE were evaluated by body weight, organ indexes, malondialdehyde (MDA), total superoxide dismutase (T-SOD), total antioxidant capacity (T-AOC), aspartate and alanine aminotransferases (AST and ALT), reactive oxygen species (ROS), mitochondrial membrane potential (MMP), hematoxylin and eosin (H&E), senescence-associated β-galactosidase (SA-β-Gal). Besides, the expressions of AMPK/SIRT1/PGC-1α and Nrf2-Keap1 were detected by Western blotting. Results: MLE could significantly prolonged nematodes' average life span and improved most physiological indicators related to aging of C. elegans. Moreover, Treatment with MLE ameliorated the decreased body weight and organ index (weight of organ/body weight) in model mice, and protected against oxidative stress in mice and liver cells, in a dose-dependent manner, up-regulating T-SOD and T-AOC, while reducing ROS and MDA levels. MLE decreased both liver and cell levels of AST and ALT, and enhanced the mitochondrial membrane potential. MLE activated the AMPK/SIRT1/PGC-1α pathways, participated in mitochondrial biosynthesis and oxidative metabolism and delayed D-gal-induced aging. MLE promoted the accumulation of Nrf2 in the nucleus, indicating that the improved oxidative stress response was mediated by the Nrf2-Keap1 pathway in vivo and in vitro. Conclusion: MLE appeared to have great potential for stimulating the oxidative stress response and attenuating the aging process of in vivo and in vitro, and provide a novel health-promoting resource against aging and aging-related diseases.
MeSH term(s)	Mice ; Humans ; Animals ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Reactive Oxygen Species/metabolism ; Galactose ; Morus ; Kelch-Like ECH-Associated Protein 1/metabolism ; Sirtuin 1/metabolism ; NF-E2-Related Factor 2/metabolism ; AMP-Activated Protein Kinases/metabolism ; Caenorhabditis elegans/metabolism ; Aging ; Oxidative Stress ; Superoxide Dismutase/metabolism ; Obesity
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Galactose (X2RN3Q8DNE) ; Kelch-Like ECH-Associated Protein 1 ; Sirtuin 1 (EC 3.5.1.-) ; NF-E2-Related Factor 2 ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2023-03-23
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.116286
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Zs.A 1494: Show issues

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Article ; Online: Tumor necrosis factor α-induced protein 8-like-2 controls microglia phenotype via metabolic reprogramming in BV2 microglial cells and responses to neuropathic pain.

Li, Yeqi / Yin, Cui / Jiang, Jinhong / Yang, Huan / Zhang, Feifei / Xing, Yanhong / Wang, Wuyang / Lu, Chen

The international journal of biochemistry & cell biology

2024 Volume 169, Page(s) 106541

Abstract: Microglial are major players in neuroinflammation that have recently emerged as potential therapeutic targets for neuropathic pain. Glucose metabolic programming has been linked to differential activation state and function in microglia. Tumor necrosis ... ...

Abstract	Microglial are major players in neuroinflammation that have recently emerged as potential therapeutic targets for neuropathic pain. Glucose metabolic programming has been linked to differential activation state and function in microglia. Tumor necrosis factor α-induced protein 8-like-2 (TNFAIP8L2) is an important component in regulating the anti-inflammatory response. However, the role of TNFAIP8L2 in microglia differential state during neuropathic pain and its interplay with glucose metabolic reprogramming in microglia has not yet been determined. Thus, we aimed to investigate the role of TNFAIP8L2 in the status of microglia in vitro and in vivo. BV2 microglial cells were treated with lipopolysaccharides plus interferon-gamma (LPS/IFNγ) or interleukin-4 (IL-4) to induce the two different phenotypes of microglia in vitro. In vivo experiments were conducted by chronic constriction injury of the sciatic nerve (CCI). We investigated whether TNFAIP8L2 regulates glucose metabolic programming in BV2 microglial cells. The data in vitro showed that TNFAIP8L2 lowers glycolysis and increases mitochondrial oxidative phosphorylation (OXPHOS) in inflammatory microglia. Blockade of glycolytic pathway abolished TNFAIP8L2-mediated differential activation of microglia. TNFAIP8L2 suppresses inflammatory microglial activation and promotes restorative microglial activation in BV2 microglial cells and in spinal cord microglia after neuropathic pain. Furthermore, TNFAIP8L2 controls differential activation of microglia and glucose metabolic reprogramming through the MAPK/mTOR/HIF-1α signaling axis. This study reveals that TNFAIP8L2 plays a critical role in neuropathic pain, providing important insights into glucose metabolic reprogramming and microglial phenotypic transition, which indicates that TNFAIP8L2 may be used as a potential drug target for the prevention of neuropathic pain.
MeSH term(s)	Humans ; Microglia/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Metabolic Reprogramming ; Neuralgia/drug therapy ; Neuralgia/metabolism ; Carrier Proteins/metabolism ; Phenotype ; Glucose/pharmacology ; Glucose/metabolism ; Lipopolysaccharides/pharmacology
Chemical Substances	Tumor Necrosis Factor-alpha ; Carrier Proteins ; Glucose (IY9XDZ35W2) ; Lipopolysaccharides
Language	English
Publishing date	2024-02-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2024.106541
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Zs.A 431: Show issues

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Article ; Online: Targeting MCOLN1/TRPML1 channels to protect against ischemia-reperfusion injury by restoring the inhibited autophagic flux in cardiomyocytes.

Sui, Zhongheng / Wang, Meng-Meng / Xing, Yanhong / Qi, Jiansong / Wang, Wuyang

Autophagy

2022 Volume 18, Issue 12, Page(s) 3053–3055

Abstract: Accumulating evidence suggests that macroautophagy/autophagy dysfunction plays a critical role in myocardial ischemia-reperfusion (I/R) injury. However, the underlying mechanisms responsible for malfunctional autophagy in cardiomyocytes subjected to I/R ... ...

Abstract	Accumulating evidence suggests that macroautophagy/autophagy dysfunction plays a critical role in myocardial ischemia-reperfusion (I/R) injury. However, the underlying mechanisms responsible for malfunctional autophagy in cardiomyocytes subjected to I/R are poorly understood. As a result, there are no effective therapeutic options that target autophagy to prevent myocardial I/R injury. We recently revealed that MCOLN1/TRPML1, a lysosomal cationic channel, directly contributes to the inhibition of autophagic flux in cardiomyocytes post I/R. We found that MCOLN1 is activated secondary to reactive oxygen species (ROS) elevation following I/R, which in turn induces the release of lysosomal zinc into the cytosol. This ultimately blocks autophagic flux in cardiomyocytes by disrupting the fusion between autophagosomes containing engulfed mitochondria and lysosomes. Furthermore, we discovered that the MCOLN1-mediated inhibition of autophagy induced by I/R impairs mitochondrial function, which results in further detrimental ROS release that directly contributes to cardiomyocyte death. More importantly, restoration of blocked autophagic flux in cardiomyocytes subjected to I/R achieved by blocking MCOLN1 channels significantly rescues cardiomyocyte death
MeSH term(s)	Mice ; Animals ; Myocytes, Cardiac/metabolism ; Autophagy ; Reactive Oxygen Species/metabolism ; Myocardial Reperfusion Injury/prevention & control ; Autophagosomes/metabolism ; Transient Receptor Potential Channels/metabolism
Chemical Substances	Reactive Oxygen Species ; Mcoln1 protein, mouse ; Transient Receptor Potential Channels
Language	English
Publishing date	2022-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2072657
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Article ; Online: MCOLN1/TRPML1 in the lysosome: a promising target for autophagy modulation in diverse diseases.

Qi, Jiansong / Li, Qingqing / Xin, Tianli / Lu, Qixia / Lin, Jinyi / Zhang, Yang / Luo, Haiting / Zhang, Feifei / Xing, Yanhong / Wang, Wuyang / Cui, Derong / Wang, Mengmeng

Autophagy

2024 , Page(s) 1–11

Abstract: MCOLN1/TRPML1 is a nonselective cationic channel specifically localized to the late endosome and lysosome. With its property of mediating the release of several divalent cations such as ... ...

Abstract	MCOLN1/TRPML1 is a nonselective cationic channel specifically localized to the late endosome and lysosome. With its property of mediating the release of several divalent cations such as Ca
Language	English
Publishing date	2024-03-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2024.2333715
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Article ; Online: Cell death modulation by transient receptor potential melastatin channels TRPM2 and TRPM7 and their underlying molecular mechanisms.

Shi, Ruixue / Fu, Yu / Zhao, Dongyi / Boczek, Tomasz / Wang, Wuyang / Guo, Feng

Biochemical pharmacology

2021 Volume 190, Page(s) 114664

Abstract: Transient receptor potential melastatin (TRPM) channels are members of the transient receptor potential (TRP) channels, a family of evolutionarily conserved integral membrane proteins. TRPM channels are nonselective cation channels, mediating the influx ... ...

Abstract	Transient receptor potential melastatin (TRPM) channels are members of the transient receptor potential (TRP) channels, a family of evolutionarily conserved integral membrane proteins. TRPM channels are nonselective cation channels, mediating the influx of various ions including Ca
MeSH term(s)	Cell Death/physiology ; Gene Expression Regulation/physiology ; Humans ; Phylogeny ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism
Chemical Substances	TRPM Cation Channels ; TRPM2 protein, human ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; TRPM7 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2021-06-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2021.114664
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Zs.A 19: Show issues

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Article ; Online: TRPML1-induced autophagy inhibition triggers mitochondrial mediated apoptosis.

Liu, Yucheng / Wang, Xinyan / Zhu, Wucheng / Sui, Zhongheng / Wei, Xiangqing / Zhang, Yang / Qi, Jiansong / Xing, Yanhong / Wang, Wuyang

Cancer letters

2022 Volume 541, Page(s) 215752

Abstract: Previous studies have demonstrated that autophagy tightly regulates apoptosis. However, the underlying mechanism whereby autophagy regulates apoptosis remains unclear. Here, we discover a "autophagy inhibition-mitochondrial turnover disruption-ROS ... ...

Abstract	Previous studies have demonstrated that autophagy tightly regulates apoptosis. However, the underlying mechanism whereby autophagy regulates apoptosis remains unclear. Here, we discover a "autophagy inhibition-mitochondrial turnover disruption-ROS elevation-DNA damage-p53 transactivation-apoptosis" axis that explicates the process of autophagy modulating apoptosis. We found that autophagy inhibition induced by TRPML1, a cationic channel localized in the lysosome, results in accumulation of damaged mitochondria via blocking the mitophagic flux to lysosomes in human melanoma and glioblastoma cells. The disrupted mitochondria turnover leads to ROS elevation, which in turn causes severe damage to DNA in these cancer cells. Damage to DNA resulted from TRPML1-mediated autophagy inhibition subsequently activates p53, which ultimately triggers mitochondrial mediated apoptosis by modulating pro- and anti-apoptosis proteins in these cancer cells. As a result, by triggering apoptosis, TRPML1-induced autophagy inhibition greatly suppresses growth of human melanoma and glioma both in vitro and in vivo. In summary, our findings define the mechanism underling the regulation of autophagy inhibition in apoptosis and represent TRPML1 as a novel target for potentially treating melanoma and glioblastoma in the clinical setting.
MeSH term(s)	Apoptosis ; Autophagy ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Humans ; Lysosomes/metabolism ; Melanoma/metabolism ; Mitochondria/metabolism ; Reactive Oxygen Species/metabolism ; Transient Receptor Potential Channels/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	MCOLN1 protein, human ; Reactive Oxygen Species ; Transient Receptor Potential Channels ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-05-26
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.215752
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Zs.A 1177: Show issues

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Article ; Online: Activity of putative orexin neurons during cataplexy.

Zhou, Shi / Yamashita, Akira / Su, Jingyang / Zhang, Yang / Wang, Wuyang / Hao, Liying / Yamanaka, Akihiro / Kuwaki, Tomoyuki

Molecular brain

2022 Volume 15, Issue 1, Page(s) 21

Abstract: It is unclear why orexin-deficient animals, but not wild-type mice, show cataplexy. The current hypothesis predicts simultaneous excitation of cataplexy-inhibiting orexin neurons and cataplexy-inducing amygdala neurons. To test this hypothesis, we ... ...

Abstract	It is unclear why orexin-deficient animals, but not wild-type mice, show cataplexy. The current hypothesis predicts simultaneous excitation of cataplexy-inhibiting orexin neurons and cataplexy-inducing amygdala neurons. To test this hypothesis, we measured the activity of putative orexin neurons in orexin-knockout mice during cataplexy episodes using fiber photometry. We created two animal models of orexin-knockout mice with a GCaMP6 fluorescent indicator expressed in putative orexin neurons. We first prepared orexin-knockout mice crossed with transgenic mice carrying a tetracycline-controlled transactivator transgene under the control of the orexin promoter. TetO-GCaMP6 was then introduced into mice via an adeno-associated virus injection or natural crossing. The resulting two models showed restricted expression of GCaMP6 in the hypothalamus, where orexin neurons should be located, and showed excitation to an intruder stress that was similar to that observed in orexin-intact mice in our previous study. The activity of these putative orexin neurons increased immediately before the onset of cataplexy-like behavior but decreased (approximately - 20% of the baseline) during the cataplexy-like episode. We propose that the activity of orexin neurons during cataplexy is moderately inhibited by an unknown mechanism. The absence of cataplexy in wild-type mice may be explained by basal or residual activity-induced orexin release, and emotional stimulus-induced counter activation of orexin neurons may not be necessary. This study will serve as a basis for better treatment of cataplexy in narcolepsy patients.
MeSH term(s)	Animals ; Cataplexy/metabolism ; Cataplexy/therapy ; Humans ; Mice ; Mice, Knockout ; Mice, Transgenic ; Narcolepsy/metabolism ; Narcolepsy/therapy ; Neurons/metabolism ; Orexins/metabolism
Chemical Substances	Orexins
Language	English
Publishing date	2022-03-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-022-00907-w
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Article ; Online: Mechanism of cell death pathways in status epilepticus and related therapeutic agents.

Du, Ke / He, Miao / Zhao, Dongyi / Wang, Yuting / Ma, Chao / Liang, Hongyue / Wang, Wuyang / Min, Dongyu / Xue, Lei / Guo, Feng

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2022 Volume 149, Page(s) 112875

Abstract: The most severe form of epilepsy, status epilepticus (SE), causes brain damage and results in the development of recurring seizures. Currently, the management of SE remains a clinical challenge because patients do not respond adequately to conventional ... ...

Abstract	The most severe form of epilepsy, status epilepticus (SE), causes brain damage and results in the development of recurring seizures. Currently, the management of SE remains a clinical challenge because patients do not respond adequately to conventional treatments. Evidence suggests that neural cell death worsens the occurrence and progression of SE. The main forms of cell death are apoptosis, necroptosis, pyroptosis, and ferroptosis. Herein, these mechanisms of neuronal death in relation to SE and the alleviation of SE by potential modulators that target neuronal death have been reviewed. An understanding of these pathways and their possible roles in SE may assist in the development of SE therapies and in the discovery of new agents.
MeSH term(s)	Cell Death ; Ferroptosis ; Humans ; Necroptosis ; Seizures ; Status Epilepticus/drug therapy
Language	English
Publishing date	2022-03-31
Publishing country	France
Document type	Journal Article ; Review
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2022.112875
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