TOXICOLOGY AND APPLIED PHARMACOLOGY
·
2025
·
IF 3.4
Ying Li,Zhi-Hao Ma,Xiao Liu,Wenting Zhu,Long Chen,Wanyi Xu,Lei Wang,Jingquan Dong,Zi-Bo Dong
Higenamine Hydrochloride (HGN) is an alkaloid derived from the traditional Chinese medicinal herb Aconite, possesses pharmacological activities such as anti-inflammatory and antioxidant properties. Its specific role in diabetic nephropathy (DN) remains unknown. The purpose of this work was to investigate the protective impact of HGN against streptozotocin (STZ)-induced renal inflammation and fibrosis in DN mice, as well as to investigate its probable mechanism of action in vitro using high glucose (HG)-treated HK-2 cells. We constructed a mouse model of DN by intraperitoneal injection of STZ and a HK-2 cell model using HG treatment, followed by administration of HGN. Tissue distribution experiments, biochemical analysis, real-time PCR, immunoblotting, and histopathological examination were used to assess the effects of HGN on renal histopathology, inflammation, and fibrosis in DN mice and its molecular mechanisms. The results demonstrated that in the renal tissues of DN mice, HGN had the highest concentration. HGN treatment led to body weight increase, and blood glucose levels fell as well as the improvement in metabolic abnormalities. It further proved that HGN alleviated renal function damage by lowering serum creatinine (SCr), blood urea nitrogen (BUN), cystatin C (Cys-C), and renal index values. Moreover, HGN improved kidney histopathology, reduced renal tubular damage, and decreased interstitial inflammation. The kidneys had less collagen accumulation. At the same time, HGN decreased the expression of markers associated with inflammation (iNOS, IL-1β, IL-6, MCP-1) and fibrosis (Collagen-I, MMP9, α-SMA, CTGF). Mechanistic studies have shown that, in vitro, HGN inhibits STAT3 phosphorylation, thereby inhibiting the expression of inflammatory (iNOS, IL-1β, IL-6, and MCP-1) and fibrosis-related cytokines (Collagen-I, MMP9, α-SMA, and CTGF) in HK-2 cells under HG conditions. To summarize, HGN inhibits renal inflammation and fibrosis in DN mice by inhibiting the STAT3 pathway, and this discovery offers a new possible target for DN treatment.
研究领域:
药理学
·
传统中医药
·
分子生物学
·
病理学
·
生物化学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FASEB JOURNAL
·
2025
·Vol. 39
·期 14
·e70861
·
IF 4.2
Ke Sun,Fugang Huang,Wenjin Xie,Wenbo Hu,Mengting Zhu,Zhenliang Fan,Keda Lu
Chronic kidney disease (CKD) is a significant global health issue, and effective treatments are limited. Xiaoyu Xiezhuo Decoction (XYXZD), a traditional Chinese medicine, has shown potential in modulating the gut–kidney axis and related signaling pathways. This study investigates the effects of XYXZD in alleviating tubulointerstitial fibrosis (TIF) in a unilateral ureteral obstruction (UUO) rat model by targeting the aldosterone (ALD)/mineralocorticoid receptor (MR)/serum- and glucocorticoid-inducible kinase-1 (SGK-1) signaling pathway and exploring the role of butyrate. UUO rats were divided into four groups: control, UUO model, XYXZD treatment, and irbesartan treatment. Renal function was assessed by measuring serum creatinine (Scr), blood urea nitrogen (BUN), and ALD levels. Fibrosis markers, including alpha-smooth muscle actin (α-SMA) and Collagen Type III (COL-III), as well as signaling molecules such as phosphorylated SGK-1 (p-SGK-1) and phosphorylated nuclear factor kappa B (p-NF-κB), were analyzed by Western blot and immunohistochemistry. Gut microbiota composition was evaluated using 16S ribosomal DNA (rDNA) sequencing, and the role of butyrate was examined via oral gavage treatment. XYXZD significantly improved renal function, reduced fibrosis, and restored gut microbiota balance by increasing butyrate-producing bacteria. XYXZD also reduced serum ALD levels and inhibited SGK-1 phosphorylation, suggesting modulation of the ALD/MR signaling pathway. Furthermore, butyrate treatment reduced MR nuclear translocation, supporting its role in the therapeutic effects of XYXZD. XYXZD alleviates renal injury in UUO rats by modulating the gut–kidney axis, particularly through the ALD/MR/SGK-1 signaling pathway, with butyrate playing a critical role. These findings highlight a promising approach for CKD treatment by targeting gut microbiota and enhancing butyrate production. Graphical Mechanism of XYXZD improvement of renal injury through modulation of the gut–kidney axis and ALD/MR/SGK-1 signaling pathway.
研究领域:
药理学
·
肾脏病学
·
微生物学
·
中医学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Meng-xiao Wang,Ke-ke Luo,Meng-yao Tian,Wen-ya Gao,Shan Jiang,Yan Zhang,Jian Yang,Nan Si,Shi-lan Ding,Xiao-lu Wei,Yu-yang Liu,Bao-lin Bian,Yan-yan Zhou,Hong-jie Wang
The diagnosis and treatment of chronic glomerulonephritis (CGN) during childhood pose distinct challenges. Acteoside (ACT) is the primary active ingredient extracted from the leaves of Rehmannia glutinosa by our research group, accounting for 2.15 %, which possess multiple biological activities, especially for nephropathy treatment. However, its mechanism intervention on CGN in children remains obscure. In this study, we established a model of purinomycin aminonucleoside (PAN)-induced CGN in childhood rats to assess the potential therapeutic effect and underlying mechanisms of ACT. Leveraging network pharmacology and multi-omics technology, we delved into the effects and mechanisms of ACT intervention on CGN. And these findings were further corroborated through qRT-PCR, western blot and targeted metabolomics. Our results demonstrated that ACT had significantly efficient in the treatment of CGN in childhood rats by improving the key indicators and pathological changes. Further, ACT could significantly regulate differences in endogenous small molecules and genes based on non-target metabolomics and transcriptomics. Meanwhile, target capture analysis found the crucial targets of ACT treatment in CGN. Integrated analysis of multi-omics study indicated that PI3K/Akt signaling pathway and its downstream amino acid metabolism were significantly enriched, hinting at the essential regulatory pathway for ACT in treating of CGN. Finally, through qRT-PCR, western blot and targeted metabolomics, it was verified that ACT could ameliorate CGN through Cxcr4-PI3K-Akt-eNOS signaling pathway, thereby regulating amino acid metabolism. The collective results were consistent with those of multi-omics analysis. Our study illuminated that ACT had notable curative effect on CGN rats, and preliminarily elucidated its mechanism of action. Our research will provide solid basis for the treatment of chronic glomerulonephritis in children with ACT and developing it into innovative traditional Chinese medicine.
研究领域:
药理学
·
分子生物学
·
肾脏病学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Drug Design Development and Therapy
·
2025
·
IF 5.1
Yijing Zhou,Chengli Lou,Xiuqin Xu,Bo Feng,Xiaoping Fan,Xiangjing Wang
Purpose Ursolic acid (UA) improves diabetic nephropathy (DN), but its regulatory mechanism requires further verification.Methods The bioactive component-target network of UA in DN was determined using a network pharmacology approach. DN mice (STZ-diabetic C57BL/6 mice, n = 8/group, 4 weeks) were treated with UA (25 mg/kg and 100 mg/kg) and the JAK agonist RO8191 (2 mg/kg). The DN cell model (high glucose-injured NRK-52E cells) was treated with UA (10 and 50 µM) and RO8191 (2 μM) for 24 h. The molecular mechanisms by which UA acts were further verified in vivo and in vitro.Results UA treatment ameliorated the general state of the DN mouse model, as characterized by the attenuation of weight loss and downregulation of fasting blood glucose (FBG) and fasting serum insulin (FINS) levels (all P < 0.05). Renal pathological changes and impaired renal function (increased levels of Scr, BUN, and UAER) were also improved by UA treatment (all P < 0.05). In vitro, UA increased the viability of DN cells in vitro (P < 0.001). Concurrently, UA remarkably downregulated the levels of ROS, SOD, and iron and up-regulated the levels of MDA, GPX4, and SLC7A11 (all P < 0.05) in vivo and in vitro. Mechanistically, activation of the JAK2-STAT3 pathway with the agonist RO8191 significantly reduced UA’s anti-ferroptosis and anti-oxidative effects of UA.Conclusion UA protected against DN by blocking JAK2/STAT3-mediated ferroptosis.
研究领域:
药理学
·
分子生物学
·
生物信息学
·
糖尿病研究
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INFLAMMATION
·
2020
·Vol. 44
·期 2
·746-757
·
IF 3.212
Gao Yang,Kang Kai,Liu Yan-song,Li Na-na,Han Qiu-yuan,Liu Hai-tao,Kong Wei-lan,Zhang Xing,Huang Rui,Yang Zhen-yu,Qi Zhi-dong,Zheng Jun-bo,Li Ming,Wang Hong-liang,Li Jia-yu,Liu Rui-jin,Wang Si-cong,Zhang Wei-hua,Zhao Ming-yan,Yu Kai-jiang
This study aimed to investigate the effect of splenectomy on dexmedetomidine-activated cholinergic anti-inflammatory pathway-mediated alleviation of LPS-induced AKI. A mouse model of septic kidney injury was established in C57BL/6 mice. A total of 30 C57BL/6 mice were randomly divided into the control group, LPS group, dexmedetomidine + LPS group, splenectomy group, splenectomy + LPS group, and splenectomy + dexmedetomidine + LPS group. The pathological effects in kidney tissues in each group were analyzed by HE staining. Apoptosis in each group was examined by the TUNEL method. Cr and Cys-C levels in each group were measured by ELISA. The expression levels of IL-6, NF-κB p65, Caspase-3, the antiapoptotic protein Bcl-2, the proapoptotic protein Bax, and α7nAChR in each group were measured by qRT-PCR and Western blotting. Dexmedetomidine alone reduced apoptosis in kidney tissue; however, apoptosis was increased after splenectomy in mice treated with dexmedetomidine. Splenectomy reduced the production of proinflammatory cytokines in circulation and had a protective effect on the kidney. Splenectomy inhibited dexmedetomidine-mediated activation of the α7nAChR pathway. Dexmedetomidine effectively alleviated LPS-induced kidney injury, and splenectomy inhibited the anti-inflammatory, antiapoptotic, and renoprotective effects of dexmedetomidine. The kidney-spleen axis is mediated by the α7nAChR-NF-κB signaling pathway and is involved in the development of AKI.
研究领域:
肾病学
·
免疫学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
BIOLOGICAL & PHARMACEUTICAL BULLETIN
·
2019
·Vol. 42
·期 6
·886-891
·
IF 1.54
Yangbiao He,Xujun Lang,Dong Cheng,Zhihao Yang
Previous studies implicated the mammalian target of rapamycin (mTOR)/hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway in renal fibrosis and found that curcumin could suppress the expression of mTOR. Therefore, the aim of the present study was to investigate the therapeutic effects of curcumin against chronic renal failure (CRF) in a rat model induced by 5/6 nephrectomy through inhibition of mTOR/HIF-1α/VEGF signaling. A total of 70 male Sprague–Dawley rats were divided into seven groups: a sham group, a CRF group, and five treatment groups. Except for the sham rats, all rats underwent 5/6 nephrectomy to induce CRF. The 5/6 nephrectomized rats received treatment with curcumin vehicle, everolimus vehicle, curcumin, everolimus, or the combination of curcumin and everolimus. Everolimus, a specific inhibitor of mTOR, was used as a positive control. At the end of treatment, blood biochemical indexes, proteinuria and the kidney index were detected. Moreover, histological change was examined by hematoxylin and eosin staining, and protein expression levels were detected by Western blotting. The blood biochemical indexes, proteinuria, and kidney index were increased in the CRF group as compared to the sham group, which was accompanied by marked activation of the mTOR/HIF-1α/VEGF pathway. However, curcumin, as well as everolimus, restored or ameliorated these changes. These results indicate that activation of the mTOR/HIF-1α/VEGF signaling pathway plays an important role in the occurrence and development of CRF, and that curcumin has renoprotective effects by blocking activation of this pathway.
研究领域:
药理学
·
肾病学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF TRACE ELEMENTS IN MEDICINE AND BIOLOGY
·
2025
·
IF 3.3
Ziyan Han,Yuzhou Zhuo,Zhihui Dai,Xinhui Zhang,Bingqian Zhu,Yuyan Liu,Zhuoyu Chai,Jiayi Wu,Lijun Chen
Background Cinnabar is a mercury-containing mineral traditionally used in Chinese medicine and can induce kidney injury via mercury toxicity. Given that cinnabar contains elements such as selenium, it is reasonable to hypothesize that its multi-element composition may regulate nephrotoxicity through intermetallic interactions. To validate this hypothesis and clarify the distinct renal toxicity between cinnabar and single mercury compounds, we compared the nephrotoxic effects of cinnabar, Zhu-Sha-An-Shen-Wan (ZSASW), mercuric sulfide (HgS), and mercuric nitrate (Hg(NO₃)₂). By co-administration with sodium selenite (Na₂SeO₃), this study related to the nephrotoxicity of cinnabar was improved from the perspective of metal-element interactions, which provided a new perspective for the safety assessment of mercury-containing medicines. Methods Mice were gavaged with 0.5 % CMC-Na solution, cinnabar (50.0 and 200 mg/kg), HgS (50.0 mg/kg), Na 2 SeO 3 (1.00 mg/kg), cinnabar (50.0 mg/kg)+Na 2 SeO 3 (1.00 mg/kg), HgS (50.0 mg/kg)+Na 2 SeO 3 (1.00 mg/kg), ZSASW (600 mg/kg), ZSASW (600 mg/kg)+Na 2 SeO 3 (1.00 mg/kg) or Hg(NO 3 ) 2 (0.900 mg/kg in Hg 2+ ) daily for 30 days. Renal histopathology was assessed by H&E staining. Related protein expression was measured by Western blotting. Renal total Hg (THg) concentration in kidney was determined by cold vapor atomic fluorescence spectroscopy. Result Western blotting revealed significantly decreased OAT1 and GPX4 levels in all experimental groups compared to the Control group ( P < 0.05). NF-κB activation occurred in the Hg(NO₃)₂, Cinnabar-H, HgS, and HgS-Na₂SeO₃ groups. Hg(NO₃)₂ administration caused a significant decline in body weight growth rate ( P < 0.001), severe renal tubular degeneration with epithelial cell swelling, and the highest renal THg concentration (773.77 % exceeding the Control group). Na₂SeO₃ alone induced inflammatory infiltration and tubular epithelial degeneration. The Cinnabar-H and HgS groups exhibited distinct renal damage (localized tubular degeneration and vascular hyaline degeneration, respectively) with elevated renal THg concentration (330.74 % and 347.95 % exceeding the Control group). The Cinnabar-L, Cinnabar-Na₂SeO₃, ZSASW, and ZSASW-Na₂SeO₃ groups maintained normal histology despite increased renal mercury content (227.46 %, 40.57 %, 67.2 %, and 556.56 % exceeding the Control group). Co-administration of Na₂SeO₃ with HgS restored OAT1 and GPX4 expression ( P < 0.001), suppressed NF-κB activation, and minimally altered renal mercury accumulation (RSD=0.45 %). Na₂SeO₃ reduced mercury levels in the cinnabar-treated mice (57.07 % reduction) but increased accumulation in ZSASW-treated mice (292.65 % increase). Conclusion This study confirms that cinnabar and ZSASW exhibit lower toxicity than mercuric sulfide or mercuric nitrate. Multi-component synergistic or antagonistic effects need to be considered when studying the mechanism of action of cinnabar-related drugs.
研究领域:
毒理学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FITOTERAPIA
·
2025
·
IF 2.6
Pei-Pei Zhang,Ming-Yang Cui,Shui-Yuan Yang,Bo Han,Wei Yu,Tian-Tian Wei,Ke-Wu Zeng,Peng-Fei Tu
Recent studies have demonstrated the therapeutic potential of Astragalus membranaceus in diabetic kidney disease (DKD); however, the underlying mechanisms remain incompletely elucidated. In this study, we established a streptozotocin-induced DKD mouse model to evaluate the effects of A. membranaceus extract (AME) on glycemic control, renal function, gut microbiota composition, and metabolic profiles. Biochemical analyzes revealed that A. membranaceus significantly attenuated hyperglycemia and improved renal function, as indicated by reduced serum creatinine and blood urea nitrogen levels. Metagenomic sequencing demonstrated that A. membranaceus reversed microbial dysbiosis by suppressing pathogenic bacteria (e.g., Aerococcus urinaeequi ) and enriching beneficial probiotics (e.g., Thomasclavelia cocleata ). Furthermore, LC/MS-based metabolomics identified key metabolic pathways, including glycerophospholipid metabolism and bile acid synthesis, as potential mediators of the therapeutic effects. These findings underscore the crucial role of the gut-renal axis in DKD pathogenesis and provide a mechanistic basis for the clinical application of A. membranaceus .
✓ 已验证
产品关联
DOI
PubMed
高影响因子
KIDNEY & BLOOD PRESSURE RESEARCH
·
2023
·Vol. 48
·期 1
·405-413
·
IF 2.8
Peng Zining,Wang Xueyi,Zhu Qing,Wang Huili,Li Bing,Pang Xinxin,Han Jiarui
Introduction: Diabetic nephropathy (DN) is a common complication in diabetic patients. Chemerin, a novel adipokine, has been associated with renal damage in DN. The chemerin chemokine-like receptor 1 (CMKLR1) has been reported to participate in DN. In this study, we aimed to investigate the effect of a CMKLR1 antagonist, 2-(anaphthoyl)ethyltrimethylammonium iodide (α-NETA), on DN. Methods: To induce diabetes, 8-week-old male C57BL/6J mice were given a single intraperitoneal injection of 65 mg/kg streptozotocin (STZ). Diabetic mice were randomly assigned to receive daily doses of 0, 5, or 10 mg/kg α-NETA for 4 weeks. Results: α-NETA dose-dependently induced body weight and reduced fasting blood glucose levels in STZ-induced diabetic mice. Furthermore, α-NETA significantly reduced the expressions of renal injury markers, including serum creatinine, kidney weight/body weight, urine volume, total proteins, and albumin in the urine, and increased creatinine clearance. Periodic acid-Schiff staining also indicated that α-NETA could effectively ameliorate renal injuries in DN mice. In addition, α-NETA inhibited renal inflammation and the expressions of chemerin and CMKLR1 in mice with DN. Conclusion: In summary, our findings suggested that α-NETA has beneficial effects on the management of DN. Specifically, α-NETA effectively ameliorated renal damage and inflammation in a dose-dependent manner in mice with DN. Thus, targeting the chemerin and CMKLR1 axis with α-NETA may be a promising therapeutic strategy for the treatment of DN
研究领域:
药理学
·
肾病学
·
糖尿病研究
✓ 已验证
DOI
PubMed
高影响因子
SENSORS AND ACTUATORS B-CHEMICAL
·
2019
·
IF 6.393
Ying Zhang,Wang Ren,Yu Zhu Fan,Hong Qun Luo,Nian Bing Li
Monitoring the concentration of norepinephrine (NE), epinephrine (Ep) and dopamine-β-hydroxylase (DβH) is of great importance in studying and diagnosing related diseases. In this study, a simple chemically-modulated turn-on fluorescence strategy is proposed for rapid, selective and visual discrimination of trace NE and Ep. Herein, Ep is differentiated from other catecholamines via its fast fluorescence response in 1.0 M NaOH medium. Furthermore, NE is alkalized with 0.01 M NaOH and is then immediately triggered by polyethyleneimine to emit bright cyan fluorescence, whereas Ep and DA show no any fluorescence response. The fluorescence intensity of resultant solution is linearly proportional to the concentration of Ep and NE in the range of 50.0–10000.0 nM and 10.0–10000.0 nM, respectively. Moreover, NE and Ep as low as 500.0 nM can be fluorescently identified with naked-eye, which is convenient for rapidly preliminary diagnosis and self-test of hypercatecholaminism. Inspired by the catalytic property of DβH transforming DA into NE, the proposed strategy enables a simple and high-efficient fluorescence method to monitor DβH by using trace DA as substrate and directly quantifying NE. The method is simple, smart, highly efficient and eco-friendly, and has been applied to the rapid assay of NE, Ep and DβH in real samples.
研究领域:
生物化学
·
医学诊断
·
分析化学
✓ 已验证
DOI
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Jianan Yang,Tonglian Jiang,Xun Lu,Xiang li,Xuling Zhou,Xinxin Guo,Chengxin Ma,Xiaobei Xie,Dongxiao Li,Siqi Yu,Jiayi An,Binghai Zhao,Hongzhi Li
Hyperuricemia is a known risk factor for chronic kidney disease (CKD) and subsequent renal fibrosis. N6-methyladenosine (m6A) is the most prevalent chemical modification in eukaryotic mRNAs and has been implicated in various diseases. However, its role in hyperuricemic nephropathy (HN) remains unclear. This study investigated the involvement of the methylase METTL14 in HN pathogenesis. Our in vitro and in vivo function experiments demonstrated that METTL14 plays a crucial role in HN. In mouse models of uric acid (UA)-induced renal injury, we detected impaired kidney function, increased renal interstitial fibrosis, and significantly decreased m6A methylation levels in renal tissues. Treatment with benzbromarone, a UA-lowering drug, alleviated renal injury, restored m6A methylation levels, and upregulated METTL14 expression. Cellular experiments showed that METTL14 overexpression attenuated high UA-induced fibrosis in renal tubular epithelial cells. This overexpression significantly decreases the expression of GLUT9, a key protein involved in UA transport, leading to reduced UA reabsorption. Additionally, MeRIP-qPCR and dual-luciferase reporter gene experiments further demonstrated that METTL14 overexpression enhanced Glut9 mRNA m6A methylation modification, accelerating its degradation and decreasing expression levels. Thus, METTL14-mediated RNA m6A modification plays a role in the renal tubular epithelial cell damage induced by high UA, by regulating Glut9 mRNA post-transcriptionally. These findings provide valuable insights for the diagnosis and development of therapeutic drugs for HN.
研究领域:
肾病学
·
分子生物学
·
表观遗传学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Human Cell
·
2025
·Vol. 38
·期 2
·1-16
·
IF 3.1
Zhang Lexi,Ye Jianfeng,Qiu Cheng
Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury (AKI). Twist-related protein 2 (Twist2) is a basic helix/loop/helix transcription factor. However, the underlying effects of Twist2 in IRI remain to be elucidated. Herein, we found that the expression of Twist2 was significantly upregulated in renal tissues of mice induced by ischemia/reperfusion (I/R) and in human renal tubular epithelial cell HK-2 exposed to hypoxia–reoxygenation. We silenced Twist2 with RNAi technology. Twist2 knockdown alleviated renal pathological damage in mice. Twist2 depletion ameliorated IRI-induced mitochondrial dysfunction, such as increasing ATP content and mitochondrial DNA copy number and restoring mitochondrial membrane potential in the kidneys of mice , and similar results were observed in in vitro experiments. Twist2 interference increased the expression of LC3B and decreased the expression of p62 and mitochondrial membrane proteins TIMM23 and TOMM20 both in vivo and in vitro. Electron microscope and the co-localization of LC3B and mitotracker DsRed suggested the induction of autophagy and mitophagy after Twist2 knockdown in kidneys or cells. Mechanism studies revealed that Twist2 exerted a direct inhibitory effect on BCL2 interacting protein 3 (Bnip3) transcriptional activity by targeting the Bnip3 promoter. In hypoxia/reoxygenation-induced renal tubular epithelial cells, the interference of Bnip3 reversed the effect of Twist2 depletion on mitochondrial function and mitophagy. In conclusion, our findings suggest that the depletion of Twist2 exerts renoprotective effect in I/R-induced AKI. Twist2 regulates mitochondrial function and mitophagy in part by targeting and downregulating Bnip3. Our study provides new insights into the pathological mechanisms of I/R-induced AKI.
研究领域:
肾病学
·
分子生物学
·
转化医学
✓ 已验证
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）