MOLECULAR AND CELLULAR BIOCHEMISTRY
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2026
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IF 4.7
Yang Chunyan,Chen Bin,Jing Haiqing,Liu Qing,Wang Yanqiong,Wu Yanrui,Song Jiayi,Fu Yi
Angiogenesis plays a significant role in the progression of idiopathic pulmonary fibrosis (IPF). The RNA-binding protein IGF2BP3 is associated with fibrosis and angiogenesis, but its role in IPF angiogenesis remain unclear. Additionally, Tianlongjie (TL) has been confirmed to inhibit IPF progression, but the role of IGF2BP3 in this process also needs to be elucidated. A bleomycin (BLM)-induced pulmonary fibrosis rat model was established via intratracheal instillation of BLM, and an angiogenesis cell model was constructed by treating HPMVECs with VEGF165. HE staining was used to detect lung tissue injury. Masson staining, HYP content measurement, Western blot, and Immunohistochemistry assessed to evaluate fibrosis and angiogenesis progression. EdU staining was employed to detect cell proliferation. RIP-qPCR and dual-luciferase reporter assays were performed to examine the interaction between IGF2BP3 and HIF-1α. IGF2BP3 was abnormally highly expressed in pulmonary fibrosis. IGF2BP3 knockdown reduced the expression of HYP, COL-I, COL-III, α-SMA, CD31, CD34, and VEGFA in pulmonary fibrosis rat lung tissues, increased E-cadherin expression, and inhibited pulmonary fibrosis progression and microvascular formation in rats. In vitro, IGF2BP3 knockdown suppressed cell proliferation, migration and vascular endothelial cell angiogenesis. Mechanistically, IGF2BP3 may promote HIF-1α stability through m 6 A modification, and HIF-1α overexpression attenuated the inhibitory effect of IGF2BP3 knockdown on angiogenesis. Furthermore, TL treatment was associated with reduced fibrosis and lower IGF2BP3/HIF-1α expression. In conclusion, IGF2BP3 can promote pulmonary fibrosis-related angiogenesis by stabilizing HIF-1α expression, and TL inhibits IGF2BP3 and HIF-1α expression, angiogenesis and fibrosis progression in pulmonary fibrosis rats.
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高影响因子
BIOCHEMICAL PHARMACOLOGY
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2025
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IF 5.6
Yueyang Guo,Zhuang Hu,Linyue Bai,Yanjun Tang,Jingyi Hu,Qianqian Zhang,Jiali Liu,Siqi Feng
Gastric cancer, a leading cause of cancer-related mortality, has a median survival of just 15 months in advanced stages and currently lacks effective treatment options. Neddylation blockade is a promising therapeutic strategy, yet its clinical application faces challenge with the emergence of drug resistance. Currently, the underlying mechanisms behind the drug resistance are not fully understood. Our study uncovers the link between MLN4924-induced metabolic reprogramming and its antitumor efficacy in gastric cancer cells. We first demonstrated that MLN4924, a neddylation blocker, has multiple effects on gastric cancer cell growth, notably inducing mitochondrial damage. Untargeted metabolomic analysis revealed that MLN4924 enhances glucose utilization in gastric cancer cells in a concentration-dependent manner. Mechanistically, MLN4924 reduces the neddylation of cullin2, thereby inhibiting the degradation of HIF-1α. This leads to the accumulation of HIF-1α, which upregulates GLUT1 levels and facilitates increased glucose uptake. This metabolic adaptation allows gastric cancer cells to maintain their energy supply despite mitochondrial impairment. Based on the increased glucose dependency following neddylation inhibition by MLN4924, we propose a co-targeting strategy with GLUT1 inhibition, which significantly improves therapeutic efficacy in vitro and in vivo models without safety risks. This dual-targeting approach represents a potent new strategy for gastric cancer treatment.
研究领域:
肿瘤学
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代谢组学
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药理学
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DOI
PubMed
高影响因子
PHYTOMEDICINE
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2023
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IF 7.9
Anni Zhu,Zhiguang Duan,Yanru Chen,Chenhui Zhu,Daidi Fan
Background The aging of skeletal muscle is the leading cause of physical disability in older adults, currently effective treatment methods are lacking. Ginsenoside Rh4, an active component extracted from ginseng , possesses beneficial anti-inflammatory and anti-oxidative effects. Purpose The aim of this study was to elucidate the antioxidant effect of ginsenoside Rh4 on aging skeletal muscle and its molecular mechanism of anti-aging of skeletal muscle. Study design In this study, we employed a D-galactose-induced model of skeletal muscle aging to investigate whether ginsenoside Rh4 can delay the process of skeletal muscle senescence. Methods The effects of ginsenoside Rh4 on oxidative damage and inflammation in aging skeletal muscle were analyzed using immunofluorescence, immunohistochemistry , ELISA kits, H&E staining, flow cytometry, and protein immunoblotting . The changes of ginsenoside Rh4 on mitochondrial morphology were observed by transmission electron microscopy , and ELISA kits and protein immunoblotting analyzed the effects of ginsenoside Rh4 on mitochondrial homeostasis in skeletal muscle cells . The influence of ginsenoside Rh4 on the SIRT1 signaling pathway in aging skeletal muscle were investigated by protein immunoblotting, immunofluorescence, and β-galactosidase staining. Results Our results showed that Rh4 improved the morphology of muscle fibers and produced an anti-inflammatory response. Furthermore, in vitro experiments indicated that ginsenosides reduced the production of senescent cells, while Rh4 effectively alleviated oxidative damage in skeletal muscle and restored mitochondrial balance. Transcriptome analysis and molecular docking showed that Rh4 improved mitochondrial homeostasis and delayed skeletal muscle aging by regulating the PGC-1α-TFAM and HIF-1α-c-Myc pathways via targeting SIRT1. Conclusion Ginsenoside Rh4 improves oxidative stress and inflammation in skeletal muscle by activating SIRT1, deacetylating Nrf2, regulating PGC-1α-TFAM and HIF-1α-c-Myc pathways, and enhancing mitochondrial homeostasis, thus achieving the effect of delaying skeletal muscle aging.
研究领域:
药理学
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老年学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 6.8
Mengjie Qiu,Xiao Zhou,Aofeng Sun,Huiwen Chen,Xuan Xu,Liuhui Zheng,Yihan Ye,Yini Xu,Xiaofan Hong,Dandan Zheng,Chengguang Zhao,Haiyang Zhao,Lehe Yang
Ethnopharmacological relevance Linderalactone is a sesquiterpene lactone isolated from Linderae Radix, a traditional Chinese medicinal herb used for pain and inflammatory disorders. Given the roles of hypoxia-related signaling, oxidative stress, and iron-dependent lipid peroxidation in fibrotic lung remodeling, linderalactone was evaluated as a natural product-derived anti-fibrotic lead. Aim of the study To evaluate the anti-pulmonary fibrosis activity of linderalactone and determine whether modulation of HIF-1α-dependent ferroptotic stress contributes to its underlying mechanism. Materials and methods BLM-induced pulmonary fibrosis mice and TGF-β1-stimulated lung fibroblasts were used. Histopathology, fibrosis markers, oxidative stress, ferroptotic stress-related markers, intracellular iron, and lipid peroxidation were assessed. HIF-1α was analyzed by immunostaining and manipulated by siRNA knockdown or DMOG-mediated stabilization. BODIPY-C11 and ferrostatin-1 were used to monitor lipid peroxidation and probe function. Results Linderalactone alleviated lung injury and collagen deposition and suppressed fibroblast-to-myofibroblast transition. HIF-1α, colocalized with α-SMA-positive myofibroblasts, was downregulated. Linderalactone reduced malondialdehyde, PTGS2, lipid peroxidation, and intracellular iron, and restored glutathione, SLC7A11/xCT, and GPX4. HIF-1α knockdown phenocopied, whereas DMOG weakened, its protective effects. Fer-1 partially suppressed fibroblast activation, supporting a functional role for ferroptotic stress. Conclusions Linderalactone alleviates experimental pulmonary fibrosis by suppressing HIF-1α signaling and attenuating HIF-1α-associated oxidative stress and ferroptotic stress. These findings support the HIF-1α–ferroptotic stress axis as a plausible mechanism, provide proof-of-concept for linderalactone as a natural product-derived anti-fibrotic candidate, and warrant further pharmacokinetic and translational investigation.
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PubMed
高影响因子
Redox Biology
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2025
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IF 11.9
Zhanliang Jiang,Jin Li,Mingpeng Shi,Yunfei Li,Ning Sun,Kai Xi,Xiangyan Li,Daqing Zhao,Xiangyang Leng,Zhenwei Zhou,Haisi Dong
Aberrant changes in the hypoxic microenvironment are implicated in osteoarthritis (OA) development. Cuproptosis, a unique copper-dependent form of regulated cell death that depends on the activity of key enzymes in mitochondrial metabolism, is also linked to oxygen levels. However, the crosstalk among hypoxic environment, cuproptosis, and OA development remains unclear. This study confirmed that oxygen levels in the OA model gradually increased during OA progression, which suppressed the expression of anabolic genes for articular cartilage extracellular matrix, upregulated catabolic genes, and increased the cell death rate of primary chondrocytes. Mechanistically, oxygen elevation upregulated the expression of solute carrier family 31 member 1 (SCL31A1), a transmembrane pump facilitating copper uptake, whereas it downregulated the expression of ATPase copper transporting beta (ATP7B), a copper chaperone facilitating copper efflux, leading to aberrant copper accumulation in the cells. Ultimately, this accumulation efficiently induces oligomerization of dihydrolipoamide S-acetyltransferase (DLAT), triggering cell death, known as cuproptosis. Hypoxia-inducible factor-1α (HIF-1α), induced under hypoxic conditions, is negatively correlated with DLAT and the severity of OA, as confirmed in human and rat cartilage. Furthermore, siRNA-mediated HIF-1α silencing sensitized primary chondrocytes to cuproptosis, whereas HIF-1α stabilization had protective effects. In summary, increased oxygen levels in the cartilage induce cuproptosis, thereby accelerating OA progression, whereas HIF-1α stabilization mitigates this process. These findings may provide novel therapeutic targets for OA treatment in clinical practice.
研究领域:
分子生物学
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病理学
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细胞生物学
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生物医学
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DOI
PubMed
高影响因子
ACS Applied Nano Materials
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2023
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IF 5.9
Jinyu An,Xue Jiang,Qian Wu,Zhiru Zou,Yingqiao Li,Junpeng Sun,Xiaobang Liu,Ying Xiong,Chao Wu,Xifan Mei,He Tian
Secondary injury following spinal cord injury (SCI) results in a large production of reactive oxygen species (ROS) (e.g., H2O2) in the spinal cord microenvironment, which then leads to an excessive burst of inflammation and ultimately neuronal death. In this study, we prepared manganese dioxide (MnO2) nanoparticles coated by macrophage membranes, named M@MnO2, to cope with early ROS bursts in the SCI microenvironment. The biosafety and targeting ability of the MnO2 nanoparticles were improved through the macrophage membranes. Successful preparation of M@MnO2 was verified by transmission electron microscopy, Western blot, and dynamic light scattering. Small animal imaging showed that M@MnO2 accumulated in large quantities at the site of SCI. In the early stages of SCI, M@MnO2 effectively reduced the ROS content, as well as the hypoxia-inducible factor 1α (HIF-1α) content, malondialdehyde content, and superoxide anion content caused by ROS, further leading to a decrease in some of the proteins associated with inflammation at the site of SCI (CD11b, CD86, COX2, IL-1β, and iNOS), ultimately achieving neuroprotection and recovery of motor function.
研究领域:
纳米技术
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神经科学
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生物材料
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药理学
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DOI
高影响因子
Journal of Ovarian Research
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2026
·Vol. 19
·期 1
·157
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IF 5.3
Wang Mei,Chen Hongling,Lin Shaozi,Meng Zuyu,Zhang Yiyao,Liu Fang,Li Menghan,Sun Chengjin,Guan Minxi,Song Lingliang,Zhao Guoping,Zhang Di,Qin Jiajia
Background Premature ovarian insufficiency (POI) is characterized by complex etiologies and currently lacks effective treatments, posing significant threats to women’s physical and psychological health. Quercetin (QUE), a bioactive flavonoid inherent in traditional herbs such as Flos Sophorae and Cuscuta chinensis, demonstrates potent redox-modulating and anti-senescence capacities. This investigation validates its therapeutic efficacy against POI, specifically elucidating granulosa cell-centric mechanisms. Methods POI mouse models and injury models of the KGN (human ovarian granulosa cell line) were induced through the administration of cyclophosphamide (CTX). Subsequently, these models were treated with drugs such as QUE. Morphological changes in the ovaries of the mice were observed, and vaginal smears were conducted to monitor the estrus cycles and patterns of the mice. ELISA was employed to detect sex hormone levels in various mouse groups, while Hematoxylin-eosin (H&E) staining was utilized to assess the status of ovarian follicles at different stages. Moving forward, immunohistochemical analysis and Western blot were conducted to detect the expression levels of Sirtuin 1 (SIRT1), Hypoxia-Inducible Factor 1 Alpha (HIF-1α), and other apoptosis-related proteins. Ultimately, methods such as Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) assay, β -galactosidase staining, flow cytometry for apoptosis detection, and 5-Ethynyl-2′-deoxyuridine (EdU) assay were utilized to evaluate the apoptosis, senescence, and proliferation of mouse ovarian tissues and human ovarian granulosa cells KGN. Results QUE alleviated CTX-induced ovarian atrophy and follicular atresia by upregulating SIRT1 expression. Furthermore, QUE partially restored estrous cyclicity, normalized sex hormone levels, and improved follicular counts through SIRT1/HIF-1α modulation. Concurrently, QUE suppressed apoptosis in both murine and human granulosa cells via the SIRT1/HIF-1α pathway. Conclusion Our findings demonstrate that QUE enhances ovarian reserve by inhibiting granulosa cells apoptosis via SIRT1/HIF-1α signaling, highlighting its therapeutic potential for POI management. Graphical The alternative text for this image may have been generated using AI.
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高影响因子
Redox Biology
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2026
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IF 16.2
Zhiying Yang,Rui Ma,Weili Wu,Ying Shi,You Chen,Xiaotong Luo,Kai Li,Liangcai Wu,Bo Wang,Boyu Zhang,Ping Yuan
The lack of effective therapeutic options available for microsatellite stable (MSS) colorectal cancer (CRC) remains a significant clinical challenge. Interestingly, chemotherapy-resistant cancer cells can be induced to undergo ferroptosis, prompting our investigation into RSL3, a potent ferroptosis inducer, in MSS CRC cells. Our findings revealed that while RSL3 suppressed the growth of MSS CRC cells, a subset displayed resistance. Single-cell sequencing uncovered an aberrant activation of hypoxia pathways in RSL3-resistant MSS CRC cells. Inhibiting HIF-1α, the key transcription factor driving hypoxia signaling, restored RSL3 sensitivity in these resistant cells; moreover, this sensitivity was attenuated upon HIF-1α overexpression. Chromatin immunoprecipitation assays further demonstrated that in RSL3-resistant cells, HIF-1α was enriched at the promoter of P4HA1, a gene implicated in ferroptosis resistance, thereby enhancing its expression. Additionally, in vivo experiments using syngeneic transplantation of CT26 cells in mice revealed that combining RSL3 with an HIF-1α inhibitor markedly enhanced tumor suppression and metastasis prevention, concomitant with increased intratumoral infiltration of CD8 + T cells and CD86 + macrophages. Notably, the combination enhanced the antitumor response of anti-PD1, a treatment otherwise ineffective on this tumor. These findings suggest that targeting HIF-1α represents a promising therapeutic strategy when used in conjunction with a ferroptosis inducer for the treatment of MSS CRC.
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DOI
PubMed
高影响因子
FREE RADICAL BIOLOGY AND MEDICINE
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2025
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IF 8.2
Wenqi Qian,Xijun Chen,Liuqing Gu,Xiangxiang Lin,Jiawei Chen,Dongchen Xu,Hao Wang,Fucai Long,Qichuan ZhuGe,Peng Zhang,Haoqi Ni
An increasing body of evidence indicates that ferroptosis, characterized by lipid peroxidation (LPO), plays a significant role in the neurophysiological and pathological changes following traumatic brain injury (TBI). Herbacetin (HBT), primarily derived from Sedum plants, is hypothesized to possess strong antioxidant activity due to the presence of five phenolic hydroxyl groups in its structure, which may allow it to counteract ferroptosis after TBI, thereby offering a potential therapeutic approach for TBI treatment. In our study, we employed an erastin and RSL3-induced ferroptosis model using HT22 and PC12 cells. Our findings demonstrated that HBT significantly mitigates erastin-induced cell death by reducing reactive oxygen species (ROS) levels, LPO, and Fe 2+ accumulation. Moreover, HBT protected against changes in mitochondrial membrane potential and mitochondrial superoxide levels induced by erastin and RSL3. We further confirmed HBT’s ability to inhibit ferroptosis in the TBI mouse model. HBT reduced the levels of LPO and iron deposition in the tissue surrounding the injury site after TBI, protected neurons, and decreased microglial activation. Mechanistically, we showed that HBT upregulates hypoxia inducible factor-1α (Hif-1α) expression in both ferroptosis cells and the TBI animal model, which in turn leads to the upregulation of recombinant solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), thereby reducing ferroptosis. RNA-seq analysis and Hif-1α knockdown experiments in HT22 cells supported this conclusion. In conclusion, our findings provide a potential therapeutic basis for the clinical use of HBT in preventing neuronal ferroptosis following TBI.
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DOI
PubMed
高影响因子
Kidney360
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2025
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IF 3
Li Jiachang,Ma Yuhan,Wang Yanni,Chen Yizhi,Wei JiaLi
Plain Language Summary Background: Hyperuricemia is a common metabolic disorder and a risk factor for multiple diseases, including CKD. Hyperuricemic nephropathy (HN) affects many individuals with hyperuricemia, yet its molecular mechanisms are not fully understood, and effective treatments are lacking. Methods: In vitro, human tubular epithelial cells (HK-2) were exposed to uric acid for 36 hours, followed by transfection with microRNA mimic or FIH-1 siRNA. In vivo, HN was induced in mice using potassium oxonate (PO) and adenine (Ad) for two weeks. miR-295 mimic or anti-miR-295 was administered via tail vein injection, and mice were sacrificed for analysis. Results: We demonstrated a significant increase of miR-295 in renal tubular cells in HN mice. Hyperuricemia led to the activation of hypoxia inducible factor-1α (HIF-1α), and inhibition of HIF-1α by YC-1 (a HIF-1α inhibitor) prevented the increase of miR-295. ChIP assay further verified HIF-1α binding to the miR-295 gene promoter directly. Functionally, Inhibition of miR-295 led to increased cell death and tubulointerstitial fibrosis in HN mice, whereas supplementation of miR-295 mimic had kidney protective effects in this model. miR-295 suppressed the expression of factor inhibiting hypoxia-inducible factor-1 (FIH-1) in both in vitro and in vivo models of HN. Luciferase microRNA target reporter assay further verified FIH-1 as a direct target of miR-295.In addition, knockdown of FIH-1 inhibits tubular cell apoptosis and profibrotic cytokines production in HK2 cells during uric acid treatment. Conclusions: This study reveals a HIF-1α/miR-295/FIH-1 positive feedback loop that regulates tubular damage and fibrosis in HN. Plain Language Summary This study explores the molecular mechanisms of hyperuricemic nephropathy (HN), a kidney condition linked to high uric acid levels. Researchers found that in mice with HN, the microRNA miR-295 increased in kidney cells. The study identified a feedback loop involving miR-295, HIF-1α, and FIH-1, where HIF-1α activates miR-295, which then suppresses FIH-1. Inhibition of miR-295 led to increased cell death and fibrosis, while supplementation with miR-295 mimic had protective effects against kidney damage. Inhibiting HIF-1α prevented miR-295 increase. These findings suggest potential therapeutic targets for treating HN by modulating this molecular pathway. Text is machine generated and may contain inaccuracies. FAQ
研究领域:
肾脏病学
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分子生物学
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代谢性疾病
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细胞信号传导
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2026
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IF 5.6
Jie Chen,Dexian Li,Xiaohu Chen,Qiuxing He,Anna Zuo,Baizhao Peng,Ying Yang,Chuanghai Wu,Qinghong Chen,Zihao Jiang,Ziwei Li,Wen Fang,Jingxin Lin,Hiu Yee Kwan,Xiaomin Sun,Lin Zhou,Xiaoshan Zhao
Limonin alleviates hyperuricemia-induced cognitive impairment and neuroinflammation in UOX −/− rat models. • Limonin exerts neuroprotective effects by inhibiting microglial activation and subsequent neuronal apoptosis. • Limonin modulates the HIF-1α/iNOS pathway to exert anti-inflammatory and neuroprotective effects. Background Hyperuricemia (HUA), a highly prevalent metabolic disorder, is increasingly linked to cognitive impairment. Limonin (LIM), a natural compound with anti-inflammatory and neuroprotective properties, has the therapeutic benefits, but its underlying mechanisms remain unclear. Purpose This study aimed to investigate the therapeutic effect and mechanism of LIM on HUA-induced cognitive impairment. Methods A rat model of HUA-induced cognitive impairment was established using urate oxidase gene knockout (UOX −/− ) rat. Uric acid (UA) levels of serum and cerebrospinal fluid (CSF) were measured to confirm hyperuricemia. Cognitive function was assessed using morris water maze test, while neuronal morphology and synaptic integrity were evaluated via Nissl staining and synaptic plasticity biomarkers. Microglial activation and polarization were examined through double immunofluorescence staining of CD86/IBA1 and ARG1/IBA1, inflammatory and oxidative stress markers were quantified using ELISA, qRT-PCR and Western blot. In vitro , BV2 microglial cells were stimulated with UA to model activation and inflammatory responses. HT22 neuronal cells were co-cultured using conditioned medium to assess apoptosis via TUNEL assay and expression of apoptosis-related biomarkers. RNA sequencing was performed to identify key signaling pathways modulated by LIM, and the findings were validated through targeted gene overexpression or inhibition experiments. Results The UOX −/− rat model successfully recapitulated HUA-induced cognitive impairment, as evidenced by elevated UA levels, alongside significant cognitive deficits. LIM treatment ameliorated these cognitive impairments, attenuated neuropathological alterations, modulated microglial M1/M2 polarization, and reduced neuroinflammation and oxidative damage. In vitro , LIM suppressed UA-induced microglial activation and inflammatory response, while also rescuing neuronal apoptosis in HT22 cells. RNA sequencing revealed involvement of the HIF-1 pathway. HIF-1α inhibitor YC-1 enhanced LIM's effects, whereas HIF-1α activator DMOG reversed them, suggesting that the modulation of the HIF-1α/iNOS pathway contributes to redox homeostasis and neuroinflammation. Conclusion LIM ameliorates HUA-induced cognitive impairment by suppressing microglial activation and neuroinflammation, which is associated with the inhibition of the HIF-1α/iNOS signaling pathway, underscoring its therapeutic potential. Download: Download high-res image (110KB) Download: Download full-size image
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高影响因子
FEBS Journal
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2026
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IF 4.2
Baopeng Tian,Jie Shen,Xuanning Chu,Yannan Zhou,Hao Li,Lei Wang,Min Guo,Jie Dou
Mitophagy, the process of removing mitochondria through the autophagy–lysosome pathway, is crucial for maintaining cellular homeostasis. However, its regulatory mechanisms and pathological implications remain poorly understood. In our study, we revealed that decidual protein induced by progesterone (DEPP) plays a significant role in mitophagy through the DEPP–HIF-1α–BNIP3/NIX axis. Our findings indicate that interaction between DEPP and hypoxia-inducible factor 1-alpha (HIF-1α) enhances HIF-1α stability, thereby promoting the transcription of HIF-1 target genes. The enhanced protein stability of HIF-1α not only activates mitophagy by stimulating the transcription of BCL2-interacting protein 3 ( BNIP3 ) and BCL2-interacting protein 3-like ( BNIP3L ; also known as NIX ) mRNA but also influences cellular metabolic reprogramming by promoting the transcription of glycolysis-related genes. In conclusion, our findings suggest that DEPP may act as a potential regulator of mitophagy and HIF-1α, playing an important role in maintaining cellular metabolic and energy homeostasis.
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PubMed
高影响因子
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