A5040284436- Mitochondrial Function and Pathology
- Trace Elements in Health
- Heavy Metal Exposure and Toxicity
- Autophagy in Disease and Therapy
- Electromagnetic Fields and Biological Effects
- Alzheimer's disease research and treatments
- Carcinogens and Genotoxicity Assessment
- Neuroscience and Neuropharmacology Research
- Paraquat toxicity studies and treatments
- MicroRNA in disease regulation
- Effects and risks of endocrine disrupting chemicals
- ATP Synthase and ATPases Research
- Heavy metals in environment
- Bone Metabolism and Diseases
- Adipose Tissue and Metabolism
- Cardiac Ischemia and Reperfusion
- Parathyroid Disorders and Treatments
- Anesthesia and Neurotoxicity Research
- Metabolism and Genetic Disorders
- Advanced biosensing and bioanalysis techniques
- Electrochemical Analysis and Applications
- Phytoestrogen effects and research
- Traditional Chinese Medicine Analysis
- Bone and Joint Diseases
- Metabolomics and Mass Spectrometry Studies
Chongqing Medical and Pharmaceutical College
2023-2025
Chongqing Medical University
2025
Nanjing Medical University
2021-2024
Jiangxi University of Traditional Chinese Medicine
2023-2024
Chongqing Public Health Medical Center
2024
Peking Union Medical College Hospital
2024
Chinese Academy of Medical Sciences & Peking Union Medical College
2024
National University of Defense Technology
2024
Chongqing University
2023
Wuhan Prevention and Treatment Center for Occupational Diseases
2023
Cadmium is one of the most toxic metal compounds found in environment. It well established that Cd induces hepatotoxicity humans and multiple animal models. Melatonin, a major secretory product pineal gland, has been reported to protect against Cd-induced hepatotoxicity. However, mechanism behind this protection remains be elucidated. We exposed HepG2 cells different concentrations cadmium chloride (2.5, 5, 10 μM) for 12 h. induced mitochondrial-derived superoxide anion-dependent autophagic...
Abstract Pathologic alterations in podocytes lead to failure of an essential component the glomerular filtration barrier and proteinuria chronic kidney diseases. Elevated levels saturated free fatty acid (FFA) are harmful various tissues, implemented progression diabetes its complications such as diabetic nephropathy. Here, we investigated molecular mechanism palmitate cytotoxicity cultured mouse podocytes. Incubation with dose-dependently increased cytosolic mitochondrial reactive oxygen...
Abstract Mitochondrial permeability transition pore (mPTP) is involved in cardiac dysfunction during chronic β-adrenergic receptor (β-AR) stimulation. The mechanism by which β-AR stimulation leads to mPTP openings elusive. Here, we show that administration of isoproterenol (ISO) persistently increases the frequency followed mitochondrial damage and dysfunction. Mechanistically, this effect mediated phosphorylation fission protein, dynamin-related protein 1 (Drp1), Ca 2+ /calmodulin-dependent...
Non-ST-segment elevation acute coronary syndrome (NSTE-ACS) is the leading cause of morbidity and mortality from cardiovascular disease worldwide. Several recent studies have shown relationship between triglyceride-glucose (TyG) index vascular disease; however, role TyG in NSTE-ACS has not been extensively assessed. Thus, we aimed to investigate association with risk factors outcomes NSTE-ACS. Overall, 438 patients were enrolled examine SYNTAX score major adverse events (MACEs). The was...
Nanozyme-based colorimetric sensors are promising approaches for environmental monitoring, food safety, and medical diagnostics. However, developing novel nanozymes that exhibit high catalytic activity, good dispersion in aqueous solution, sensitivity, selectivity, stability is challenging. In this study, the first time, single-atom iridium-doped carbon dot (SA Ir-CDs) synthesized via a simple situ pyrolysis process. Doping dots with iridium form of single atoms to achieve maximum atomic...
The effect of bisphenol A (BPA) on the reproductive system is highly debated but has been associated with meiotic abnormalities. However, evidence lacking regard to mechanisms involved. In order explore underlying BPA-induced abnormalities in adult male rats, we exposed 9-week-old Wistar rats BPA by gavage at 0, 2, 20 or 200 μg/kg body weight (bw)/day for 60 consecutive days. 17β-Estradiol (E2) was administered 10 bw/day as estrogenic positive control. Treatments and E2 significantly...
Mitochondria are critical targets in the hepatotoxicity of cadmium (Cd). Abnormal mitochondrial dynamics have been increasingly implicated dysfunction pathophysiological conditions. Therefore, our study aimed to investigate effects and underlying mechanism Cd on during hepatotoxicity. In L02 liver cell lines, 12 μM chloride (CdCl2) exposure induced excessive fragmentation as early 3 h post-treatment with Cd, which preceded such reactive oxygen species (ROS) overproduction, membrane potential...
How cadmium (Cd) induces mitochondrial loss in the context of its hepatotoxic effects remains enigmatic. The purpose study was to investigate whether mitophagy contributes cadmium-induced hepatotoxicity and determine potential mechanism. In normal human liver L02 cells, we observed that Cd treatment led a significant increase LC3-II formation, number GFP-LC3 puncta lysosomal colocalization with mitochondria. These results were associated bioenergetic deficit. Additionally, abrogation...
Abstract Cadmium (Cd) is a persistent environmental toxin and occupational pollutant that considered to be potential risk factor in the development of neurodegenerative diseases. Abnormal mitochondrial dynamics are increasingly implicated damage various neurological pathologies. The aim this study was investigate whether disturbance contributed Cd‐induced neurotoxicity melatonin has any neuroprotective properties. After cortical neurons were exposed 10 μ M cadmium chloride (CdCl 2 ) for...
Melatonin is an indolamine synthesized in the pineal gland that has a wide range of physiological functions, and it been under clinical investigation for expanded applications. Increasing evidence demonstrates melatonin can ameliorate cadmium-induced hepatotoxicity. However, potentially protective effects against hepatotoxicity underlying mechanisms this protection remain unclear. This study investigates pretreatment on elucidates potential mechanism melatonin-mediated protection. We exposed...
Calcium (Ca2+) is a key regulator of energy metabolism. Impaired Ca2+ homeostasis damages mitochondria, causing cardiomyocyte death, pathological hypertrophy, and heart failure. This study investigates the regulation role mitochondrial uniporter (MCU) in chronic stress-induced cardiac remodeling.MCU knockout or transgenic mice were infused with isoproterenol (ISO; 10 mg/kg per day, 4 weeks). Cardiac hypertrophy remodeling evaluated by echocardiography histology. Primary cultured rodent adult...
Abstract Cadmium (Cd) is a high‐risk pathogenic toxin for hepatic diseases. Excessive mitophagy hallmark in Cd‐induced hepatotoxicity. However, the underlying mechanism remains obscure. Mitochondrial calcium uniporter (MCU) key regulator mitochondrial and cellular homeostasis. Here, Cd exposure upregulated MCU expression increased Ca 2+ uptake are found. inhibition through siRNA or by Ru360 significantly attenuates excessive mitophagy, thereby rescues dysfunction increases hepatocyte...
Cadmium (Cd) is a neurotoxic contaminant that induces cognitive decline similar to observed in Alzheimer's disease (AD). Autophagic flux dysfunction attributed the pathogenesis of AD, and this study aimed investigate effect autophagy on environmental Cd-induced AD progression underlying mechanism. Here, Cd exposure inhibited autophagosome-lysosome fusion impaired lysosomal function, leading defects autophagic clearance then APP accumulation nerve cell death. Proteomic analysis coupled with...
Nickel is a potential neurotoxic pollutant. Oxidative stress supposed to be involved in the mechanism underlying nickel-induced neurotoxicity. Melatonin has efficient protective effects against various oxidative damages nervous system. The purpose of this study was investigate whether melatonin could efficiently protect neurotoxicity induced by nickel. Here, we exposed primary cultured cortical neurons and mouse neuroblastoma cell lines (neuro2a) different concentrations nickel chloride...
Endothelial progenitor cell (EPC) differentiation is considered crucial for vascular repair. Vascular endothelial growth factor (VEGF) induces EPC differentiation, but the underlying mechanism of this phenomenon remains unclear. Connexin 43 (Cx43) reported to be involved in regulation stem differentiation. Therefore, we sought determine whether Cx43 VEGF-induced and Rat spleen-derived EPCs were cultured treated with various concentrations VEGF (0, 10, or 50 ng/mL), relationship between...
SIRT1 is a multifaceted NAD+-dependent protein deacetylase known to act as tumor promoter or suppressor in different cancers. Here, we describe novel mechanism of SIRT1-induced hepatocellular carcinoma (HCC) metastasis. overexpression was frequently detected human HCC specimens and associated with microvascular invasion (P = 0.0039), advanced node metastasis (TNM) stages 0.0016), recurrence 0.021) poor outcomes 0.039). Lentivirus-mediated knockdown MHCC97H cells reduced vitro vivo. depletion...
Cadmium (Cd), a highly ubiquitous heavy metal, induces neurotoxicity. Melatonin, major secretory product of the pineal gland, protects against Cd-induced However, mechanism that accounts for this protection remains to be elucidated. Herein, we exposed mouse neuroblastoma cells (Neuro-2a cells) different concentrations cadmium chloride (CdCl2 ) (12.5, 25, and 50 μ mol L(-1) 24 hours. We showed Cd inhibits autophagosome-lysosome fusion impairs lysosomal function, subsequently leading nerve...
Mitochondrial Ca2+ homeostasis is crucial for balancing cell survival and death. The recent discovery of the molecular identity mitochondrial uniporter pore (MCU) opens new possibilities applying genetic approaches to study regulation in various types, including cardiac myocytes. Basal tyrosine phosphorylation MCU was reported from mass spectroscopy human mouse tissues, but signaling pathways that regulate entry through posttranslational modifications are completely unknown. Therefore, we...