Journal of Orthopaedic Surgery and Research
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2023
·Vol. 18
·期 1
·1-15
·
IF 2.6
Xue Xiang,Dai Tianming,Chen Junyan,Xu Yangyang,Yang Zhenyu,Huang Jian,Xu Wuyan,Li Siming,Meng Qingqi
Background Osteoarthritis (OA) is a prevalent disease plaguing the elderly. Recently, chondrocyte ferroptosis has been demonstrated to promote the progression of OA. Peroxisome proliferator-activated receptor-γ (PPARγ) is an important factor in maintaining cartilage health. However, the relationship between PPARγ and chondrocyte ferroptosis in OA and its mechanism is completely unclear.Methods We established a surgically induced knee OA rat model to investigate PPARγ and chondrocyte ferroptosis in OA. Rat knee specimens were collected for Safranin O/Fast Green staining and immunohistochemical staining after administered orally placebo or pioglitazone (PPARγ agonist) for 4 weeks. We used RSL3 to establish a chondrocyte ferroptosis model cultured in vitro to study the role of PPARγ activation toward ferroptosis, mitochondrial function, and PTEN-induced putative kinase 1 (Pink1)/Parkin-dependent mitophagy. GW9662 (PPARγ antagonist), Mdivi-1 (mitophagy inhibitor), and chloroquine (mitophagy inhibitor) were employed to investigate the mechanism of PPARγ-Pink1/Parkin-dependent mitophagy in the inhibition of ferroptosis.Results We found that PPARγ activation by pioglitazone attenuated not only OA but also inhibited the expression of the ferroptosis marker acyl-CoA synthetase long-chain family member 4 (ACSL4) at the same time in rats. Furthermore, in vivo and in vitro data indicated that PPARγ activation restored Pink1/Parkin-dependent mitophagy, improved mitochondrial function, inhibited chondrocyte ferroptosis, and delayed the progression of OA.Conclusion sThe present study demonstrated that PPARγ activation attenuates OA by inhibiting chondrocyte ferroptosis, and this chondroprotective effect was achieved by promoting the Pink1/Parkin-dependent mitophagy pathway.
研究领域:
骨科
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细胞生物学
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药理学
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PubMed
高影响因子
PHYTOTHERAPY RESEARCH
·
2026
·
IF 8.1
Lin Liu,Zonghui Xu,Shujing Wu,Man Li,Ruoan Wei,Mpofu Uphakeme Inobubele Sitholumusa,Junqiu Liu,Guoyin Kai
Astragaloside IV (AS-IV), a primary bioactive component of Astragalus membranaceus (AM). It is very effective in regulating renal diseases. However, the possible underlying mechanism of AS-IV on renoprotection remains unclear. The aim of this study is to find out the regulation mechanism of AS-IV on ischemia/reperfusion injury-induced Acute kidney injury (IRI-AKI). At first, AS-IV was confirmed to significantly alleviate renal dysfunction, inflammation, and renal tubular epithelial cell apoptosis in IRI-AKI mice. Then, it was found that AS-IV alleviated mitochondrial dysfunction and renal tubular epithelial cell injury induced by IRI. Growing evidence has suggested that PINK1/Parkin-mediated mitophagy plays a critical protective role in IRI. Based on this, we hypothesized that AS-IV might exert renoprotective effects through activating the PINK1/Parkin mitophagy pathway. After 3-MA inhibition of autophagy, AS-IV no longer showed its protective effect on HK-2 cells in a hypoxic environment. Through further molecular docking, cell thermal migration, and gene targeted silencing experiments, we confirmed that AS-IV activates the PINK1/Parkin mitophagy pathway and ultimately alleviates IRI-AKI. In summary, all these comprehensive experimental findings indicated that AS-IV can be used as a functional food for the prevention of renal ischemia/reperfusion injury.
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BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
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2025
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IF 4.2
Yonggang Ma,Na Luo,Chenguang Yue,Qiannan Sun,Yangyang Wang,Hongyan Zhao,Ruilong Song,Hui Zou,Jiaqiao Zhu,Zongping Liu
Background: Mitochondrial dysfunction caused by metabolic stress is a key part of diabetic nephropathy. Dapagliflozin exerts significant hypoglycemic and nephroprotective effects; however, the precise mechanisms underlying its renoprotective actions remain to be fully elucidated. Objective: This study aimed to elucidate the molecular mechanisms through which dapagliflozin mitigates diabetic nephropathy (DN), with particular emphasis on its regulatory role in the Sirt1-Pink1-Parkin axis and the restoration of mitochondrial homeostasis via mitophagy. Methods: Rats were fed a high-fat/high-sugar diet and streptozotocin. They were then divided into groups of various treatments. In vitro, high glucose-induced NRK-52E cell injury was treated with dapagliflozin. Evaluations included renal histopathology, urinary biomarkers, apoptosis, reactive oxygen species, mitochondrial membrane potential, and Sirt1/Pink1/Parkin pathway activation. Results: Dapagliflozin exerted significant protective effects against streptozotocin-induced diabetic nephropathy. Dapagliflozin treatment in vitro restored mitochondrial membrane potential and reduced ROS levels in high glucose-induced NRK-52E cells. High glucose exposure markedly upregulated the expression of mitochondria-associated apoptotic proteins in NRK-52E cells, which was reduced by dapagliflozin. This study revealed that Sirt1/Pink1/Parkin-mediated mitophagy was suppressed in DN and high glucose-induced NRK-52E cells but was activated following dapagliflozin treatment. Conclusion: Our findings demonstrate that dapagliflozin modulates Sirt1/Pink1/Parkin-mediated mitochondrial autophagy and effectively restores mitochondrial homeostasis in diabetic nephropathy. Modulating mitochondrial autophagy through this pathway may serve as a promising therapeutic strategy for diabetic nephropathy.
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2024
·Vol. 25
·期 21
·11695
·
IF 4.9
Jiachen Shi,Zeping Ji,Xu Yao,Yujie Yao,Chengyun Li,Qijun Liang,Xiaohui Zhang
Heat shock protein 90 (HSP90) is recognized for its protective effects against heat stress damage; however, the specific functions and underlying molecular mechanisms of HSP90 in heat-stressed cardiomyocytes remain largely unexplored, particularly in tropical species. In our study, Wenchang chickens (WCCs) were classified into two groups: the heat stress survival (HSS) group and the heat stress death (HSD) group, based on their survival following exposure to heat stress. Heat stress resulted in significant cardiomyocyte damage, mitochondrial dysfunction, and apoptosis in the HSD group, while the damage was less pronounced in the HSS group. We further validated these findings in primary cardiomyocytes derived from Wenchang chickens (PCWs). Additionally, heat stress was found to upregulate Pink1/Parkin-mediated mitophagy, which was accompanied by an increase in HSP90 expression in both cardiomyocytes and PCWs. Our results demonstrated that HSP90 overexpression enhances PINK1/Parkin-mediated mitophagy, ultimately inhibiting apoptosis and oxidative stress in heat-stressed PCWs. However, the application of Geldanamycin (GA) reversed these effects. Notably, we discovered that HSP90 interacts with Beclin-1 through mitochondrial translocation and directly regulates mitophagy levels in PCWs. In summary, we have elucidated a novel role for HSP90 and mitophagy in regulating heat stress-induced acute cardiomyocyte injury.
研究领域:
分子生物学
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细胞生物学
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应激生理学
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兽医学
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PubMed
高影响因子
PHYTOMEDICINE
·
2022
·
IF 6.656
Zhiguo Mao,Liyu Tian,Jiao Liu,Qian Wu,Ning Wang,Guangyun Wang,Yang Wang,Saiwang Seto
Background Mitophagy plays a critical role in cerebral ischemia/reperfusion by timely removal of dysfunctional mitochondria. In mammals, PINK1/Parkin is the most classic pathway mediating mitophagy. And the activation of PINK1/Parkin mediated mitophagy exerts neuroprotective effects during cerebral ischemia reperfusion injury (CIRI). Ligustilide (LIG) is a natural compound extracted from ligusticum chuanxiong hort and angelica sinensis (Oliv.) diels that exerts neuroprotective activity after cerebral ischemia reperfusion injury (CIRI). However, it still remains unclear whether LIG could attenuates cerebral ischemia reperfusion injury (CIRI) through regulating mitophagy mediated by PINK1/Parkin. Purpose To explore the underlying mechanism of LIG on PINK1/Parkin mediated mitophagy in the hippocampus induced by ischemia reperfusion. Methods This research used the middle cerebral artery occlusion and reperfusion (MCAO/R) animal model and oxygen-glucose deprivation and reperfusion (OGD/R) as in vitro model. Neurological behavior score, 2, 3, 5-triphenyl tetrazolium chloride (TTC) staining and Hematoxylin and Eosin (HE) Staining were used to detect the neuroprotection of LIG in MCAO/R rats. Also, the levels of ROS , mitochondrial membrane potential (MMP) and activities of Na + -K + -ATPase were detected to reflect mitochondrial function. Moreover, transmission electron microscope (TEM) and fluorescence microscope were used to observe mitophagy and the western blot was performed to explore the changes in protein expression in PINK1/Parkin mediated mitophagy. Finally, exact mechanism between neuroprotection of LIG and mitophagy mediated by PINK1/Parkin was explored by cell transfection. Results The results show that LIG improved mitochondrial functions by mitophagy enhancement in vivo and vitro to alleviate CIRI. Whereas, mitophagy enhanced by LIG under CIRI is abolished by PINK1 deficiency and midivi-1, a mitochondrial division inhibitor which has been reported to have the function of mitophagy, which could further aggravate the ischemia-induced brain damage, mitochondrial dysfunction and neuronal injury. Conclusion LIG could ameliorate the neuronal injury against ischemia stroke by promoting mitophagy via PINK1/Parkin. Targeting PINK1/Parkin mediated mitophagy with LIG treatment might be a promising therapeutic strategy for ischemia stroke.
研究领域:
神经科学
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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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高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2025
·
IF 4.7
Ziyi Song,Yucheng Gao,Jiangkai Yu,Yang Zhang,Wenbin Xuan,Yijun Rong,Youheng Zhang,Zengxin Gao
This study investigates the role of calreticulin (CRT) in intervertebral disc degeneration (IVDD) and elucidates its underlying mechanisms. CRT expression was markedly reduced in degenerated disc tissues, implicating its involvement in IVDD pathogenesis. Both in vitro and in vivo experiments were conducted to assess the effects of CRT on nucleus pulposus cell (NPC) pyroptosis, apoptosis, and mitochondrial function. Functional analyses demonstrated that CRT overexpression alleviated disc degeneration, inhibited pyroptotic cell death, and preserved mitochondrial integrity. Mechanistically, CRT promoted the clearance of damaged mitochondria through PINK1/Parkin-mediated mitophagy, restoring mitochondrial homeostasis and suppressing ROS accumulation and NLRP3 inflammasome activation. In vivo studies using an IVDD animal model further validated these protective effects, showing reduced disc degeneration and maintenance of extracellular matrix integrity. Recent studies have demonstrated the protective effect of CRT in IVDD. This study builds on these findings and investigates a novel mechanism through which CRT mediates its protective effects in IVDD. Specifically, our study identifies the involvement of PINK1/Parkin-mediated mitophagy in CRT's ability to preserve mitochondrial function and mitigate inflammation in NPCs, offering new insights into the molecular pathways underlying CRT's protective role in IVDD.
研究领域:
分子生物学
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细胞生物学
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骨科学
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炎症研究
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高影响因子
Hepatobiliary & Pancreatic Diseases International
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2025
·
IF 4.4
Han-Ying Zhou,Ting Li,Yuan-Qiang Lu
Background Diquat, a commonly employed bipyridyl herbicide, is recognized for its hepatotoxic effects attributed to the generation of reactive oxygen species. Baicalin (BAI), a flavonoid derivative, has garnered significant research interest for its hepatoprotective properties. Nevertheless, the clinical application of BAI is constrained by its limited water solubility and poor bioavailability. To address these challenges, BAI-nanoliposome (BAI-NL) has emerged as a novel drug delivery platform aimed at enhancing therapeutic outcomes. Methods We used diquat-induced liver injury mouse model and AML12 hepatocytes to test the protective effect of BAI and BAI-NL on liver inflammation, oxidative stress, and mitochondrial function. The parameters included histological, biochemical, and molecular biological analyses. Results In the diquat-induced model, both BAI and BAI-NL exhibited effectiveness on attenuating liver inflammation. Ex vivo analyses further indicated that BAI-NL was superior to BAI in preserving mitochondrial membrane potential, reducing oxidative stress, and modulating the phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin RBR E3 ubiquitin-protein ligase (Parkin) signaling pathway. These findings enhanced mitophagy and facilitated the removal of damaged mitochondria. Conclusions BAI-NL exhibited superior hepatoprotective effects compared to free BAI, possibly by reducing inflammation, preserving mitochondrial homeostasis, and reinstating autophagic balance through modulation of the PINK1/Parkin signaling pathway. These outcomes indicate a groundbreaking method for addressing liver diseases and underscore the potential of nanoliposome technology in augmenting the efficacy of natural compounds.
研究领域:
药理学
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毒理学
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生物化学
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分子生物学
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高影响因子
Toxins
·
2022
·Vol. 14
·期 9
·641
·
IF 5.075
Jiehuan Xu,Lingwei Sun,Mengqian He,Shushan Zhang,Jun Gao,Caifeng Wu,Defu Zhang,Jianjun Dai
Mitochondria hold redox homeostasis and energy metabolism as a crucial factor during oocyte maturation, while the exposure of estrogenic mycotoxin zearalenone causes developmental incapacity in porcine oocyte. This study aimed to reveal a potential resistance of phytoalexin resveratrol against zearalenone during porcine oocyte maturation and whether its mechanism was related with PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy. Porcine oocytes were exposed to 20 μM zearalenone with or without 2 μM resveratrol during in vitro maturation. As for the results, zearalenone impaired ultrastructure of mitochondria, causing mitochondrial depolarization, oxidative stress, apoptosis and embryonic developmental incapacity, in which mitophagy was induced in response to mitochondrial dysfunction. Phytoalexin resveratrol enhanced mitophagy through PINK1/Parkin in zearalenone-exposed oocytes, manifesting as enhanced mitophagy flux, upregulated PINK1, Parkin, microtubule-associated protein light-chain 3 beta-II (LC3B-II) and downregulated substrates mitofusin 2 (MFN2), voltage-dependent anion channels 1 (VDAC1) and p62 expressions. Resveratrol redressed zearalenone-induced mitochondrial depolarization, oxidative stress and apoptosis, and accelerated mitochondrial DNA copy during maturation, which improved embryonic development. This study offered an antitoxin solution during porcine oocyte maturation and revealed the involvement of PINK1/Parkin-mediated mitophagy, in which resveratrol mitigated zearalenone-induced embryonic developmental incapacity.Keywords:zearalenone;mitophagy;resveratrol;PINK1/Parkin;porcine oocyteKey Contribution:The application of phytoalexin resveratrol redresses oocyte developmental incapacity against zearalenone contamination. PINK1/Parkin-mediated mitophagy is involved in the antitoxin effect of resveratrol.
研究领域:
生殖生物学
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毒理学
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分子生物学
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JOURNAL OF ETHNOPHARMACOLOGY
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2026
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IF 6.8
Deng Yu,Tao Yongjian,Qing Yali,Wang Jianwei,Jie Chuanhong
Ethnopharmacological relevance Diabetic retinopathy (DR) is a severe microvascular complication of diabetes that is closely associated with hyperglycemia-induced mitochondrial dysfunction. Lishui Xiaozhong granules (LSXZ) are an empirical traditional Chinese medicine used to treat DR. However, its precise molecular targets and underlying mechanisms remain unclear. Aim of the study This study investigated whether LSXZ protects retinal cells under hyperglycemic conditions by regulating PINK1/Parkin-mediated mitophagy. Materials and methods Human Müller cells were exposed to high glucose (HG; 50 mM) to establish an in vitro model and treated with LSXZ-containing serum and the mitophagy inhibitor cyclosporin A (CsA). Genetic knockdown via siRNA was performed to validate the necessity of the PINK1/Parkin pathway. A zebrafish DR model was induced using an HG, high-fat diet, and treated with different LSXZ concentrations. Cell viability, mitophagy, apoptosis, ferroptosis, mitochondrial function, and ultrastructural changes were assessed using CCK-8 assays, western blotting, qPCR, immunofluorescence, and transmission electron microscopy. Retinal histopathology, vascular diameter, inflammatory cell activation, oxidative stress, and gene expression profiles in zebrafish were assessed using hematoxylin–eosin staining, fluorescence microscopy, and transcriptomic sequencing. Results LSXZ treatment reversed pathological changes by restoring PINK1/Parkin signaling, elevating LC3-II/LC3-I ratio, enhancing mitochondrial function, and suppressing apoptosis and ferroptosis—effects partially attenuated by CsA. Mitophagosomes increased after LSXZ treatment. Crucially, specific knockdown of PINK1 or Parkin significantly abolished LSXZ-induced cytoprotection, reversing the regulation of apoptotic/ferroptotic markers and mitochondrial recovery, thereby confirming the pivotal necessity of this pathway. In zebrafish, LSXZ alleviated hyperglycemia-induced retinal inner nuclear layer thinning, vascular dilation, excessive macrophage/astrocyte activation, and oxidative stress. These protective effects were mediated through upregulation of the TOMM40/TOMM20–PINK1/Parkin–MFN2 axis.
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高影响因子
Foods
·
2025
·Vol. 14
·期 24
·4173
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IF 5.1
Cuicui Zhuang,Jinhui Zhao,Xinying Zhang,Mingyue Guo,Yiguang Lu,Ting Pei,Yangfei Zhao,Chen Liang,Jianhai Zhang
Long-term excessive fluoride intake from food causes skeletal fluorosis, which manifests as bone sclerosis, deformation, joint dysfunction, and even disability. Mitophagy and ion homeostasis regulate bone function. This study investigated the role of melatonin (MLT) in mitigating this condition, given its known involvement in bone remodeling and the fact that fluoride impairs its synthesis in the pineal gland. Firstly, network pharmacology and molecular docking identified mitophagy as MLT’s key pathway against sodium fluoride (NaF)-induced osteosclerosis. Subsequently, a 400 mg/kg/day body weight NaF exposure model in chicken model with 25 mg/kg/day body weight MLT intervention were established in the current study. Fluoride exposure caused the disturbance of ion homeostasis, and the impairment of mitochondria and activation of PTEN-induced putative kinase1 (PINK1)/E3 ubiquitin ligase Park2 (Parkin)-mediated mitophagy in the bone. Importantly, these deleterious effects were significantly restored by MLT supplementation. In conclusion, NaF causes bone injury via ion homeostasis disruption, osteoblast mitochondrial damage, leading to excessive mitophagy. MLT inhibits fluoride-induced mitophagy through the calcium ion flow-mediated PINK1/Parkin pathway, mitigating bone damage. This study can not only ensure the safety of animal-derived food but also provide a theoretical basis for the prevention and treatment of fluorosis in humans and animals.
研究领域:
毒理学
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骨生物学
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分子药理学
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内分泌学
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线粒体研究
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DOI
PubMed
高影响因子
PHYTOMEDICINE
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2025
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IF 8.3
Lu Bocheng,Chen Yongfu,Cai Junjie,Li Ziqi,Guo Lina,Qu Tingli,Tang Li,Zheng Qian
Objective Guzhi Zengsheng Zhitong Decoction (GZZD) is a classic traditional Chinese medicine (TCM) prescription for treating knee osteoarthritis (OA), and has been widely used in clinical practice in China. Given that Forkhead box protein O 1 (FoxO1) has been identified as a potential therapeutic target for OA treatment, this study investigates the chondroprotective effects of GZZD through FoxO1-mediated mitochondrial regulation, bridging traditional medicine with contemporary molecular insights. Methods The therapeutic effects of GZZD on OA and its chondroprotective mechanisms were evaluated both in vivo and in vitro . A rat model of knee OA was established by intra-articular injection of monosodium iodoacetate (MIA), while an in vitro OA model was induced by IL-1β stimulation in chondrocytes. Histological staining, immunohistochemistry, and Western blot analyses were performed to assess cartilage protection. Serum ingredients of GZZD were identified using LC-MS/MS, and the core pathways involved in GZZD-mediated chondroprotection were explored through transcriptomics and network pharmacology. Key protein expression was examined, and molecular biology techniques were applied to validate the role of FoxO1 and its downstream pathways in regulating chondrocyte autophagy, apoptosis, and mitochondrial dysfunction. Additionally, molecular docking and molecular dynamics simulations were conducted to analyze interactions between bioactive compounds and FoxO1. Results GZZD significantly ameliorated MIA-induced knee joint damage, reduced cartilage degradation and subchondral bone destruction, and decreased OARSI scores. Treatment with GZZD markedly decreased serum levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) while enhancing protective autophagy in chondrocytes. Furthermore, GZZD inhibited chondrocyte apoptosis and mitochondrial dysfunction, accompanied by the upregulation of the cartilage matrix protein COL2A1 and the anti-apoptotic protein BCL2, along with downregulation of catabolic factors (MMP13, IL-1β). Mechanistically, GZZD activated the FoxO1/PINK1/Parkin pathway, restoring mitochondrial homeostasis and mitigating mitochondrial-dependent apoptosis, ultimately protecting chondrocytes from OA-related damage. Conclusion For the first time, this study demonstrates that the traditional Chinese medicine formula GZZD alleviates osteoarthritis by activating the FoxO1/PINK1/Parkin pathway, thereby restoring mitochondrial function and protecting chondrocytes from injury. These findings not only establish GZZD as a promising complementary therapy for OA but also provide a scientific foundation for developing FoxO1-targeted therapeutics.
研究领域:
中医中药
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分子生物学
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药理学
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风湿病学
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线粒体生物学
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系统生物学
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计算生物学
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高影响因子
MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·432
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IF 5.5
Lin Jinyu,You Bowen,Yang Xin,Li Xue,Sun Wenjuan,Xu Zhongyu,Zhang Yi,Tong Xuhui,Dong Shuying
Cerebral ischemia/reperfusion injury (CIRI) refers to the secondary brain injury that occurs when blood supply is restored to ischemic cerebral tissue, and represents one of the primary causes of adult disability and mortality. Current evidence indicates that aesculin exhibits antioxidative and anti-inflammatory activities; however, its therapeutic effects on CIRI remain to be elucidated. The objective of this study was to investigate the potential role of Esculin (ESCU) in protecting against CIRI and to elucidate its underlying mechanisms. Adult male mice were used to establish the middle cerebral artery occlusion/reperfusion (MCAO/R) model. The mice were administered varying doses of ESCU or a reference positive control drug. To evaluate the neuroprotective effects of ESCU, neurological deficit scores were assessed, and cerebral blood flow was measured. 2,3,5-triphenyltetrazolium chloride staining, H&E staining, and Nissl staining were used to determine neuronal damage. NLRP3-related markers and mitophagy-related markers were determined to investigate the mechanism of action of ESCU. ESCU afforded robust neuroprotection in mice, ameliorating functional deficits, reducing infarct size, and preserving neuronal structure. It potently alleviated oxidative stress and restored mitochondrial function (reduced ROS, improved cristae morphology, and increased mitochondrial membrane potential). Mechanistically, ESCU activated mitophagy (upregulating LC3Ⅱ, PINK1, and Parkin; downregulating p62) and inhibited the NLRP3 inflammasome (downregulating NLRP3, GSDMD-N, cleaved caspase-1, IL-1β, and IL-18). Notably, the mitophagy inhibitor Mdivi-1 abolished ESCU’s inhibition of the NLRP3 pathway, establishing a causal relationship. Thus, ESCU mitigates cerebral ischemia-reperfusion injury by coordinately enhancing mitophagy and suppressing NLRP3 inflammasome activation. Our study demonstrates that ESCU attenuates CIRI mechanistically by promoting PINK1/Parkin-mediated mitophagy, thereby suppressing NLRP3 inflammasome activation. These findings not only elucidate a novel pathway underlying ESCU’s neuroprotection but also position it as a promising therapeutic candidate for CIRI, warranting further investigation into its precise targets and clinical potential.
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