EXPERIMENTAL EYE RESEARCH
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2025
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IF 2.7
Xiangyu Liu,Meiyu Wang,Zhenzhen Ji,Xuanlin Zhu,Jinchang Tian,Yingxin Chen,Jun Cai,Mei Dong,Zhijian Li
Cataracts are one of the primary causes of blindness worldwide; however, their pathogenesis remains unclear. Oxidative stress and apoptosis are two dominant inducers in the progression of cataracts; however, little is known about the specific mechanisms associated with mitophagy. This study aimed to investigate the role of PTEN-induced putative kinase 1(PINK1)-mediated mitophagy in cataract development. Initially, we induced a rat cataract model using sodium selenite and observed the upregulated expression of PINK1 and other autophagy-related proteins within lens epithelial cells, accompanied by apoptosis. Furthermore, the survival rate of human lens epithelial cells was significantly reduced by H 2 O 2 treatment. However, PINK1 overexpression reduced ROS levels, allowing cells to survive. This reduction in reactive oxygen species (ROS) levels led to a decrease in cleaved caspase-3 and Bcl-2-associated X protein (Bax) expression and an increase in B-cell lymphoma 2 (Bcl-2) levels. In summary, PINK1 maintains mitochondrial functional stability and inhibits apoptosis by activating mitophagy, thus potentially playing a crucial protective role in cataract pathogenesis.
研究领域:
细胞生物学
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医学
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DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2025
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IF 4.2
He Li,Peipei Meng,Yuhang Meng,Yige Yang,Wensheng Zheng,Hongdong Huang,Zhigang Zhao
Renal fibrosis represents a critical pathological hallmark in progressive chronic kidney disease (CKD), yet effective therapeutic strategies remain elusive. Emerging evidence suggests that impaired mitophagy contributes to its pathogenesis. This study investigated whether ruxolitinib alleviates renal fibrosis by enhancing PINK1/Parkin-mediated mitophagy. Network pharmacology was employed to explore the potential regulatory mechanisms of ruxolitinib in renal fibrosis treatment, revealing that ruxolitinib might exert therapeutic effects through modulation of inflammation, oxidative stress and mitophagy. Subsequent in vivo and in vitro studies demonstrated that ruxolitinib treatment not only attenuated renal fibrosis progression but also reduced inflammatory responses and oxidative stress while enhancing mitophagic activity. Mechanistically, the enhancement of mitochondrial autophagy and the amelioration of renal fibrosis by ruxolitinib might be mediated via the PINK1/Parkin pathway. These results suggest that ruxolitinib may ameliorate renal fibrosis by activating PINK1/Parkin-mediated mitophagy, providing new perspectives for CKD therapeutic development.
研究领域:
药理学
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细胞生物学
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肾脏病学
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DOI
PubMed
高影响因子
Biomolecules
·
2025
·Vol. 15
·期 5
·647
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IF 4.8
Fengyu Xie,Jing Zhou,Bingshu Liu,Lijun Zhao,Cunqi Lv,Qiong Zhang,Lin Yuan,Dianjun Sun,Wei Wei
Fluoride exposure has been shown to affect immune cell subsets and immune function, but its impact on macrophage polarization remains unclear. This study investigates the effects of low fluoride exposure on macrophage polarization and its underlying mechanisms through epidemiological surveys, animal experiments, and in vitro cell experiments. In the population-based epidemiological survey, we used mass cytometry to assess the impact of low fluoride exposure (0.570–2.027 mg/L) in the environment on human immune cell populations following the current water improvement and fluoride reduction measures. A rat fluorosis model was established by treating rats with sodium fluoride (NaF) in drinking water at concentrations of 0 mg/L, 5 mg/L, 10 mg/L, 25 mg/L, and 50 mg/L for 90 days., and morphological changes were assessed by hematoxylin–eosin (H&E) staining and transmission electron microscopy in the spleen of rats. Flow cytometry was used to analyze the proportion of macrophage subtypes in the spleen, while Western blot and immunofluorescence were performed to detect the expression of mitochondrial autophagy-related proteins. An M1 macrophage model was constructed in vitro by inducing THP-1 cells, and the effects of fluoride on macrophage-related cell markers and cytokines were assessed using flow cytometry and ELISA, respectively, following intervention with an autophagy inhibitor. Mitochondrial membrane potential and mitochondrial–lysosomal colocalization are analyzed through flow cytometry and confocal microscopy. The study aims to investigate the role of mitophagy in sodium fluoride-induced macrophage polarization. Epidemiological investigations revealed that low fluoride increases the proportion of blood monocytes, as well as the expression levels of CD68 (a macrophage surface marker), CD86 (an M1 macrophage marker), and the inflammatory cytokine IFN-γ in peripheral blood mononuclear cells (PBMCs). In the rats of NaF-treated groups, splenic tissues exhibited inflammatory infiltration, mitochondrial swelling, and increased autophagosome formation. Moreover, low fluoride activated the PINK1/Parkin-mediated mitophagy pathway, promoting an increase in the M2/M1 macrophage ratio. In vitro experiments further confirmed that autophagy inhibitors reversed the NaF-induced increase in the M2/M1 macrophage ratio. This study demonstrates that low fluoride induces inflammatory responses in the body and drives M1 macrophage polarization toward M2 macrophages via mitophagy. These findings highlight the potential immunological risks associated with low fluoride and provide mechanistic insights into the interplay among fluoride, mitophagy, and macrophage polarization.
研究领域:
免疫学
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细胞生物学
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环境医学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Dongchen Xu,Chenyu ShenTu,Chuhong Zong,Weiliang Fu,Jiawei Ling,Ping Shao,Xuesong Liu,Yong Chen,Tengfei Xu
Ethnopharmacological relevance Salvia miltiorrhiza Bunge, a traditional Chinese medicine, has been utilized in the treatment of Parkinson's disease (PD) for thousands of years, as evidenced by its inclusion in ancient formulas such as YangXue XingNao Tang and XingGan ZhenFeng Tang . However, the underlying mechanisms of its therapeutic effects on PD remain unclear. Aim of the study This study aims to evaluate the therapeutic effects of Salvia miltiorrhiza Bunge on a rotenone-induced PD rat model and elucidate its mechanism of action. Methods To explore the efficacy of Salvia miltiorrhiza Bunge extract (SME) in PD, we employed both in vitro and in vivo models using rotenone-induced PC12 cells and rats. Therapeutic effects were assessed through cell viability assays, behavioral tests, and immunohistochemistry. Proteomic analysis and molecular docking experiments were conducted to identify the pathways involved in SME's effects. Immunofluorescence and Western blotting were used to validate the role of mitophagy, while transmission electron microscopy (TEM) provided direct evidence of mitophagy induction by SME. Results Salvia miltiorrhiza Bunge significantly improved motor dysfunction and mitigated dopaminergic neuron degeneration in the substantia nigra of rotenone-exposed rats. Proteomic analysis revealed significant activation of the PINK1/Parkin pathway following SME treatment. Furthermore, molecular experiments confirmed that SME induces mitophagy, which protects PC12 cells from rotenone-induced damage. Conclusion This study demonstrates the therapeutic efficacy of Salvia miltiorrhiza Bunge in mitigating PD-related pathologies. Through proteomic and molecular analyses, we identified SME's ability to activate the PINK1/Parkin pathway and promote mitophagy, offering new insights into its mechanism of action in PD.
研究领域:
药理学
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神经科学
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蛋白质组学
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DOI
PubMed
高影响因子
SCIENCE OF THE TOTAL ENVIRONMENT
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2023
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IF 9.8
Xijuan Chao,Dezhi Yao,Chuxuan Chen,Zhiguo Sheng,Benzhan Zhu
Tetrabromobisphenol A (TBBPA), as a widely used brominated flame retardant , has been implicated as a potential neurotoxicant. However, the mechanism of TBBPA-induced neurotoxicity has not been fully elucidated yet. In this study, using mouse hippocampal neuron cell HT22 as the in vitro model, the neuronal cytotoxicity of TBBPA and the mechanism by focusing on mitophagy have been studied. We found that neuronal cytotoxic effects were indeed induced by TBBPA exposure at concentrations of >20 μM for 24 h, including decreased cell viability (to 92.38 % at 20 μM; 18.25 % at 80 μM), enhanced ROS (enhanced 53.26 % at IC 50 of 60 μM, compared with that in the control group) and mitochondrial ROS (mtROS) levels (enhanced 24.12 % at 60 μM), reduced mitochondrial membrane potential (MMP) (decreased 33.60 % at 60 μM). As a protective mechanism in cells, autophagy was initiated; however, mitophagy was inhibited, where PINK1 (PINK1-Parkin activation is critical in the depolarized MMP-induced mitophagy) expression was found to be repressed and decreased, further leading to the failure of Parkin recruitment to the damaged mitochondria. Mitophagy activator, nicotinamide mononucleotide (β-NMN) that activates the PINK1-Parkin pathway, could alleviate TBBPA-induced mitophagy deficiency and further reduce the neuronal cytotoxicity, demonstrating that TBBPA-induced PINK1-Parkin-mediated mitophagy deficiency contributed to the neuronal cytotoxicity. Furthermore, we found TBBPA caused the upregulation of Atf3 ( activating transcription factor 3 ) gene transcription and expression levels, alongside reduced Pink1 levels; whereas enhanced Pink1 transcript levels were observed after ATF3 depletion even under TBBPA treatment, demonstrating TBBPA-induced overexpression of ATF3 should be responsible for the reduced PINK1 expression. Therefore, for the first time, here we demonstrate that TBBPA can inhibit PINK1-Parkin-mediated mitophagy via upregulating ATF3 expression, which further contributes to its neuronal cytotoxicity. This study should be able to improve our understanding of the mechanism of TBBPA-induced neuronal cytotoxicity.
研究领域:
毒理学
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神经科学
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细胞生物学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2022
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IF 5.195
Zuqing Su,Hongxia Li,Zeting Ye,Ying Zhu,Bing Feng,Lipeng Tang,Guangjuan Zheng
Ethnopharmacological relevance Qidan Tiaozhi capsule (QD), a traditional Chinese medicine , has been used to treat metabolic syndrome for over a decade. However, the mechanism of QD in the treatment of metabolic syndrome is still unknown. Aim of the study Growing studies demonstrate that impaired mitophagy is one of the important causes of metabolic syndrome. Thus, this research aims to investigate the mechanism of mitophagy in the QD treatment of metabolic syndrome. Materials and methods Network pharmacology and molecular docking were used to probe the mechanism of QD treatment of metabolic syndrome. In an oleic acid-induced cell model, glucose consumption and uptake capacity, triglyceride (TG), total cholesterol (TC), malonaldehyde (MDA), superoxide dismutase (SOD) and ROS levels, and mitochondrial membrane potential (MMP) were examined. mRFP-GFP-LC3 adenovirus and GFP-LC3 lentivirus were used to examine the effect of QD on mitophagy. The IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were also determined. What's more, the PINK1 gene was silenced to verify the above findings. In a high-fat diet-fed mouse model, body weight, organ indexes, OGTT, ITT, HOMA-IR, insulin sensitivity, serum MDA, SOD, TC, TG, LDL-C and HDL-C, hepatic TC, TG, LDL-C and HDL-C levels, hepatic steatosis , and IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were investigated. Results Results from network pharmacology and molecular docking suggested that QD might suppress oxidative stress to improve metabolic syndrome. In an oleic acid-induced cell model, compared with the model group, enhanced glucose consumption and uptake ability, inhibited intracellular lipid accumulation, TC, TG, MDA and ROS levels, and increased SOD level and MMP were found in QD groups. And mitophagy levels, IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were promoted. Interestingly, PINK1 silencing reversed the therapeutic action of QD on oleic acid-induced cells. In high-fat diet-fed mice, inhibited body weight, abdominal fat indexes, liver indexes, HOMA-IR, serum and hepatic TC, TG and LDL-C, serum MDA and hepatic steatosis, and increased insulin sensitivity, serum and hepatic HDL-C, serum SOD, and activated IRS2-PI3K and AMPK/PINK1-Parkin signal pathways were found in QD groups. Conclusion QD activates AMPK/PINK1-Parkin-mediated mitophagy to suppress oxidative stress to treat metabolic syndrome.
研究领域:
民族药理学
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代谢生物学
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分子生物学
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DOI
PubMed
高影响因子
Journal of Orthopaedic Surgery and Research
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2025
·Vol. 20
·期 1
·1-17
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IF 2.8
Zhang Yang,Gao Yucheng,Liu Shuanggong,Yang Guowei,Rong Yijun,Wu Dongjin,Gao Zengxin
Background Intervertebral disc degeneration (IVDD) is a multifactorial disorder and a leading contributor to chronic low back pain (LBP), highlighting the need for novel therapeutic strategies. Recent studies indicate that ferroptosis, driven by oxidative stress, plays a key role in the loss of nucleus pulposus cells (NPCs) during IVDD. Vacuole membrane protein 1 (VMP1), a membrane-associated regulator of autophagy, is known to influence various cellular processes. However, its role in IVDD remains unclear. This study investigates the function of VMP1 in IVDD and the mechanisms involved.Methods We established a rat model of IVDD to investigate the correlation between VMP1 expression and ferroptosis during IVDD progression. In vitro, a ferroptosis model of NPCs was induced using tert-butyl hydroperoxide (TBHP) to examine the effects of VMP1 knockdown on NPC apoptosis, extracellular matrix (ECM) degradation, ferroptosis, PINK1/Parkin-dependent mitophagy, and mitochondrial function. Furthermore, cyclosporin A (CsA), a mitophagy inhibitor, was employed to explore the role and potential mechanisms of VMP1 overexpression in regulating PINK1/Parkin-mediated mitophagy, mitochondrial function, and ferroptosis.Results In this study, we observed a significant downregulation of VMP1 expression in a rat model of IVDD, which was accompanied by the occurrence of ferroptosis. Subsequent experiments revealed that VMP1 knockdown aggravated apoptosis and ECM degradation in NPCs. Furthermore, we demonstrated that VMP1 silencing promoted ferroptosis, inhibited PINK1/Parkin-dependent mitophagy, and impaired mitochondrial function in NPCs. In contrast, VMP1 overexpression enhanced PINK1/Parkin-mediated mitophagy, mitigated mitochondrial dysfunction, and suppressed ferroptosis. Notably, these protective effects were abolished by treatment with CsA.Conclusion sThis study demonstrates that VMP1 alleviates IVDD by inhibiting ferroptosis and mitochondrial dysfunction in NPCs, a protective effect mediated through the promotion of PINK1/Parkin-dependent mitophagy. Our study underscores the pivotal role of VMP1 in coordinating mitophagy and ferroptosis during IVDD pathogenesis, identifying VMP1 as a potential therapeutic target for IVDD treatment.Graphical
研究领域:
生物医学
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细胞生物学
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遗传学
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DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2022
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IF 3.322
Zi-Xin Xu,Jing-Ze Li,Qin Li,Ming-Yi Xu,Hui-Yi Li
Background Increasing evidences have confirmed the relationship between mitophagy and nonalcoholic steatohepatitis (NASH). The exact mechanism of upstream circular RNAs (circRNAs) regulating PTEN-induced putative kinase 1 (PINK1) mediated mitophagy and its contribution to NASH-related liver fibrosis was explored in our study. Methods Primary hepatic stellate cells (PHSCs) from C57BL/6 mice transfected with small interfering RNAs against PINK1 (si-PINK1) and negative control (si-NC) were prepared to perform circRNA sequence. Differentially expressed circRNAs, bioinformatic analysis and predicting software were performed to select axis of circ608/miR-222/PINK1. The expressions of circ608/miR-222/PINK1 were verified by RT-qPCR. The mitochondrial function was evaluated by immunofluorescence staining of COX4 and LC3B. Results PINK1-mediated mitophagy was inhibited in NASH-related liver fibrosis mice. CircRNA sequence revealed there were 37 DE-circRNAs between si-PINK1 PHSCs and si-NC PHSCs. Bioinformatic analysis showed these DE-circRNAs were related to enriched signaling pathways (such as Wnt, Rap1, mTOR, Hippo) regulating liver fibrosis and mitophagy. Circ608 was significantly down-regulated in lipotoxic HSCs and in livers of NASH-related liver fibrosis mice. MiR222 was identified to be the target miRNA of circ608 and was negatively regulated by circ608 in lipotoxic HSCs. MiR222 also had a binding site with PINK1 and could negatively regulate PINK1. So, the axis of circ608-miR222-PINK1 was proved to participate in NASH-related liver fibrosis by regulating mitophagy. These results illustrated that circ608 might promote PINK1-mediated mitophagy though inhibiting miR222 in lipotoxic HSCs. Conclusion Circ608 could promote PINK1-mediated mitophagy of HSCs though inhibiting miR222 in NASH-related liver fibrosis.
研究领域:
分子生物学
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细胞生物学
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肝病学
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基因组学
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DOI
PubMed
高影响因子
FOOD AND CHEMICAL TOXICOLOGY
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2025
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IF 3.5
Yue Che,Xiaozhu Wang,Qian Li,Xiyi Peng,Zhen Liu,Wenhui Xu,Mei Jing,Ting Wang,Jian Gao,Weiling Wang
A B S T R A C T Exposure to 4-vinylcyclohexene diepoxide (VCD) has been associated to reproductive toxicity, However, the dynamic ovarian function alterations over time in rats and the underlying mechanisms remain unclear. This study investigated the effects of VCD on ovarian function in female Sprague-Dawley (SD) rats on the 25, 60 and 135 days after VCD injection and discovered related mechanisms. Our results showed that VCD had little ovotoxicity on the 25 th day, as no significant changes were observed except for the reduction of preantral follicles. However, on the 60 th day and 135 th day, rats exhibited irregular estrous cycles, abnormal serum sex hormone levels, ovarian morphological damage, decreased primordial and preantral follicles, and increased atretic follicles. We further found that on the 60 th and 135 th day, VCD might exert ovotoxicity by decreasing antioxidant enzyme levels, inhibiting of the Kelch-like ECH-associated protein 1 (KEAP1)/nuclear factor erythroid 2-related factor 2 (NRF2) and PTEN-induced putative kinase 1 (PINK1)/E3 ubiquitin ligase (Parkin) signaling pathway. Interestingly, on the 25 th day, KEAP1/NRF2 and PINK1/Parking signaling pathway were activated. This study provided a wider application in using laboratory rodents as a model of ovarian failure and highlighted that VCD-induced ovotoxicity was linked to the regulation of the KEAP1/NRF2 and PINK1/Parkin signaling pathways.
研究领域:
生殖毒理学
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分子生物学
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DOI
PubMed
高影响因子
POULTRY SCIENCE
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2023
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IF 4.4
Chen Yang,Pei Luo,You-tian Yang,Xin-liang Fu,Bing-xin Li,Xu Shen,Dan-ning Xu,Yun-mao Huang,Yun-bo Tian,Wen-jun Liu
ABSTRACT The mitochondrial quality control system is crucial in maintaining cellular homeostasis during environmental stress. Granulosa cells are the main cells secreting steroid hormones, and mitochondria are the key organelles for steroid hormone synthesis. The impact of the mitochondrial quality control system on granulosa cells’ steroid hormone synthesis and survival under heat stress is still unclear. Here, we showed that acute heat stress induces mitochondrial damage and significantly increases the number of mitophagy-like vesicles in the cytoplasm of duck ovary granulosa cells at the ultra-structural level. Meanwhile, we also found heat stress significantly increased mitochondrial fission and mitophagy-related protein expression levels both in vivo and in vitro . Furthermore, by confocal fluorescence analysis, we discovered that LC3 was distributed spot-like manner near the nucleus in the heat treatment group, and the LC3 spots and lysosomes were colocalized with Mito-Tracker in the heat treatment group. We further detected the mitophagy-related protein in the cytoplasm and mitochondria, respectively. Results showed that the PINK1 protein was significantly increased both in cytoplasm and mitochondria, while the LC3-Ⅱ/LC3-Ⅰ ratio increase only occurred in mitochondrial. In addition, the autophagy protein induced by acute heat treatment was effectively inhibited by the mitophagy inhibitor CysA. Finally, we demonstrated that the alteration of cellular mitophagy by siRNA interference with Drp1 and PINK1 inhibited the steroid synthesis of granulosa cells and increased cell apoptosis. Study provides strong evidence that the Drp1 regulated PINK1-dependent mitophagy pathway protects follicular granulosa cells from acute heat stress-induced injury.
研究领域:
细胞生物学
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内分泌学
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应激生理学
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DOI
PubMed
高影响因子
HISTOLOGY AND HISTOPATHOLOGY
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2025
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IF 2
Ke Wu,Chao Yu,Ping Li,Nannan Li
This study aimed to explore the beneficial effects and underlying protection mechanism of Tanshinone IIA (TSIIA) in diabetic cardiomyopathy (DCM) from the perspectives of mitophagy and mitochondrial integrity. Here, we found that TSIIA significantly increased STZ-induced body weight (L-TSIIA, 299.5 vs. 276.3; H-TSIIA, 308.3 vs. 276.3) and reduced blood glucose concentration (H-TSIIA, 16.1 vs. 21.5). Meanwhile, TSIIA effectively restored the function and morphology of myocardial tissue in diabetes mellitus (DM) rats. Further, TSIIA has been confirmed to have a protective effect on the ultrastructure and function of myocardial mitochondria, which was achieved through activation of mitophagy, as evidenced by enhanced co-localization of LC3 and COX IV (H-TSIIA, 88188.0 vs. 14829.0). Mechanistically, TSIIA alleviated DCM via activation of the PINK1/Parkin axis, increasing PINK1 (H-TSIIA, 0.5 vs. 0.2), Parkin (H-TSIIA, 0.6 vs. 0.3), Beclin-1 (H-TSIIA, 0.6 vs. 0.2) and LC3II/I (H-TSIIA, 0.5 vs. 0.3) expression, as well as decreasing p62 (H-TSIIA, 1.4 vs. 3.6) expression. This study provided a novel insight into the protective effect of TSIIA in DCM and revealed, for the first time, that TSIIA could noticeably improve STZ-induced DCM by enhancing PINK1-Parkin dependent mitophagy.
研究领域:
药理学
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心脏病学
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分子生物学
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内分泌学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
GENE
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2025
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IF 2.4
Hao Song,Minhao Xie,Hui Xu,Jianhui Liu,AnXiang Su,YiZhou Liu,Ye Wang,Yongjiao Wang,Fei Pei,Wenjian Yang
Capsaicin (CAP), a major natural functional component in chili peppers, has garnered considerable attention for its health benefits, including lipid-lowering effects, and its precise mechanisms remain unclear. This study aims to investigate the lipid-reducing effects of CAP on oleic acid (OA)-induced lipid accumulation in HepG2 cells and explore the underlying mechanisms. The results showed that CAP exerted lipid-lowering effects by reducing triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and increasing high-density lipoprotein cholesterol (HDL-C) in OA-induced HepG2 cells. CAP modulated the relative expression levels of lipid metabolism-related genes, including ACC, PPAR-α, PPAR-γ, Fasn, CPT-1, SREBP-1C, and SCD-1 in HepG2 cells. Notably, CAP activated the PINK1/Parkin-mediated mitophagy pathway to alleviatie lipid accumulation. Treatment with the mitophagy inhibitor Mdivi-1 reversed the lipid-lowering effect of CAP, and silencing PINK1 gene using siRNA abolished lipid-lowering effect of CAP in HepG2 cells, confirming the critical involvement of the pathway. In conclusion, CAP targeted the PINK1 gene and activated the PINK1/Parkin signaling pathway to promote mitophagy, restoring cellular energy homeostasis and regulating lipid synthesis and degradation, ultimately reducing lipid accumulation. These findings provided a mechanistic basis for the potential use of CAP in developing novel natural therapies for lipid metabolic disorders and obesity management.
研究领域:
药理学
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细胞生物学
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分子生物学
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生物化学
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营养科学
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产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）