BIOCHEMICAL PHARMACOLOGY
·
2025
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IF 5.6
Huimin Kong,Yao Wang,Dandan Song,Haohui Zhao,Zhihong Zhuo
Epilepsy is a chronic brain disorder characterized by recurrent epileptic seizures, which are caused by abnormal discharges of neurons in the brain. The Vav guanine nucleotide exchange factor (Vav1) has been reported to modulate inflammation and neuronal apoptosis; however, its role in epilepsy remains elusive. This study aimed to investigate the specific function of Vav1 in epileptogenesis and its underlying molecular mechanisms. Rats were challenged with lithium chloride-pilocarpine (LiCl-Pilo) treatment to induce epilepsy model. It was found a high expression of Vav1 in hippocampal tissue of epileptic rats. Vav1 knockdown reduced seizure frequency and mortality in epileptic rats. Besides, LiCl-Pilo treatment-induced spontaneous recurrent seizures was inhibited by Vav1 downregulation, as well as epileptic activity and abnormal sprouting of mossy fibers. We also showed that interfering with the expression of Vav1 alleviates seizure-induced cognitive impairment. Vav1 knockdown restrained neuronal damage and degeneration. Moreover, Sirtuin 1 (Sirt1) was found to regulate the histone acetylation of Vav1 promotor. Sirt1 activation increased the neuronal activity and decreased the neuronal apoptosis, while Vav1 overexpression reversed it. Additionally, the results of mRNA-seq indicated that Vav1 is related to neuronal function and apoptosis regulation. Our study demonstrated that Vav1 accelerates the development of epilepsy, and neuronal damage might be the critical event. These findings could provide a novel direction for epilepsy therapy.
研究领域:
神经科学
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分子生物学
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癫痫研究
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细胞信号传导
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Liangrong Wu,Chenchen Qian,Weiqi Zhang,Mengyun Shi,Xiuxiu Chen,Yi Wang,Feng Lin
Background Ginkgo biloba L., a kind of traditional Chinese medicine, is always used to treat various diseases. Ginkgetin is an active biflavonoid isolated from leaves of Ginkgo biloba L., which exhibits diverse biological activities, including anti-tumor, anti-microbial, anti-cardiovascular and cerebrovascular diseases, and anti-inflammatory effects. However, there are few reports on the effects of ginkgetin on ovarian cancer (OC). Hypothesis/Purpose OC is one of the most common cancers with high mortality in women. The purpose of this study was to find out how ginkgetin inhibited OC and which signal transduction pathways was involved to suppress OC. Methods The OC cell lines, A2780, SK-OV-3 and CP70, were used for in vitro experiments. MTT assay, colony formation, apoptosis assay, scratch wound assay and cell invasion assay were used to determine the inhibitory effect of ginkgetin. BALB/c nude female mice were injected with A2780 cells subcutaneously, then treated with ginkgetin by intragastric administration. Western blot experiment was used to verify the inhibitory mechanism of OC in vitro and in vivo . Results We found that ginkgetin inhibited the proliferation and induced apoptosis in OC cells. In addition, ginkgetin reduced migration and invasion of OC cells. In vivo study showed that ginkgetin significantly reduced tumor volume in the xenograft mouse model. Furthermore, the anti-tumor effects of ginkgetin were associated with a down regulation of p-STAT3, p-ERK and SIRT1 both in vitro and in vivo . Conclusion Our results suggest that ginkgetin exhibits anti-tumor activity in OC cells via inhibiting the JAK2/STAT3 and MAPK pathways and SIRT1 protein. Ginkgetin could be a potential candidate for the treatment of OC.
研究领域:
肿瘤学
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药理学
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分子生物学
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中药学
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产品关联
DOI
PubMed
高影响因子
AMERICAN JOURNAL OF CHINESE MEDICINE
·
2021
·Vol. 49
·期 03
·705-718
·
IF 4.667
Jiaqi Zhang,Cheng Hu,Xiulong Li,Li Liang,Mingcai Zhang,Bo Chen,Xinhua Liu,Dicheng Yang
Acetaminophen (APAP) overdose is the leading cause of acute liver failure (ALF) in the Western world, with limited treatment opportunities. 3,5,7,4 ′ -Tetrahydroxyflavanone (Dihydrokaempferol, DHK, Aromadendrin) is a flavonoid isolated from Chinese herbs and displays high anti-oxidant and anti-inflammatory capacities. In this study, we investigated the protective effect by DHK against APAP-induced liver injury in vitro and in vivo and the potential mechanism of action. Cell viability assays were used to determine the effects of DHK against APAP-induced liver injury. The levels of reactive oxygen species (ROS), serum alanine/aspartate aminotransferases (ALT/AST), liver myeloperoxidase (MPO), and malondialdehyde (MDA) were measured and analyzed to evaluate the effects of DHK on APAP-induced liver injury. Western blotting, immunofluorescence staining, RT-PCR, and Transmission Electron Microscope were carried out to detect the signaling pathways affected by DHK. Here, we found that DHK owned a protective effect on APAP-induced liver injury with a dose-dependent manner. Meanwhile, Western blotting showed that DHK promoted SIRT1 expression and autophagy, activated the NRF2 pathway, and inhibited the translocation of nuclear p65 (NF- κ B) in the presence of APAP. Furthermore, SIRT1 inhibitor EX-527 aggravated APAP-induced hepatotoxicity when treating with DHK. Molecular docking results suggested potential interaction between DHK and SIRT1. Taken together, our study demonstrates that DHK protects against APAP-induced liver injury by activating the SIRT1 pathway, thereby promoting autophagy, reducing oxidative stress injury, and inhibiting inflammatory responses.
研究领域:
药理学
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肝病学
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分子生物学
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毒理学
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DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2026
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IF 5.4
Qin Peng,Ling Xiao,Xinhui Huang,Ziyuan Huang,Guangxian Zhang,Jihong Zhou,Yuhui Tan
Chemoresistance driven by pro-survival autophagy remains a major obstacle in hepatocellular carcinoma (HCC) treatment. Berbamine (BBM), a natural alkaloid with a favorable clinical safety profile, shows potential as an autophagy inhibitor, yet its precise mechanism in HCC remains unclear. Using CCK-8, colony formation, and apoptosis assays, we first demonstrated that BBM synergistically enhanced the efficacy of multiple chemotherapeutic agents (5-FU, Sorafenib, Paclitaxel) against HCC cells in vitro . This synergistic effect was confirmed in an H22 xenograft mouse model in vivo . To investigate the mechanism, we monitored autophagic flux and lysosomal function. Western blot and immunofluorescence analyses revealed that BBM treatment led to the concurrent accumulation of LC3-II and p62, indicating a blockade of late-stage autophagic flux. Further experiments, including LysoTracker staining and assessment of lysosomal protease levels, showed that BBM impaired both autophagosome-lysosome fusion and lysosomal acidification. Mechanistically, we found that BBM downregulated SIRT1 protein expression and reduced the intracellular NAD + /NADH ratio, thereby inhibiting SIRT1 deacetylase activity. This suppression impaired the nuclear translocation and function of the key autophagy transcription factor TFEB, leading to decreased levels of its downstream targets RAB7, CTSB, and CTSD. Crucially, rescue experiments using specific agonists revealed that SIRT1 activation completely reversed all BBM-induced effects, including autophagic flux blockade and downstream protein suppression, whereas TFEB activation only partially rescued the expression of RAB7, CTSB, and CTSD without restoring autophagic flux. This establishes SIRT1 as the primary upstream regulator in this pathway. Our study identifies BBM as a novel autophagy inhibitor that targets the SIRT1-TFEB axis to disrupt autolysosomal fusion and degradation, and nominates it as a promising combinational agent to overcome chemoresistance in HCC.
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DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2025
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IF 8.3
Wei Zhang,Wenting Zhu,Xiao Liu,Silong Yuan,Da Li,He Huang,Xiaoming Huang,Lei Wang,Honggang Zhang
Background The pathogenesis of sepsis-induced cardiomyopathy (SIC) remains unclear, presenting a complex challenge in both clinical practice and research. Gypenoside XLIX (Gyp-XLIX) has garnered significant attention for its anti-inflammatory, antioxidant, and various other pharmacological activities; however, its protective effect on SIC has not been thoroughly investigated. Purpose This study aims to explore the effect of Gyp-XLIX on SIC and its potential therapeutic mechanisms. Methods A sepsis mouse model was established through cecal ligation and puncture surgery and treated with Gyp-XLIX. The modeling was evaluated through sepsis model scoring, survival analysis, weight changes, wet-to-dry weight ratio, H&E staining, biochemical assays and cardiac ultrasound. The mechanism exploration was deteced using proteomics sequencing, Western blotting, qPCR, biochemical analysis, and reactive oxygen species assays. Additionally, target proteins of Gyp-XLIX were identified through LC-MS/MS proteomics analysis, molecular docking, CESTA, DARTS, SPR with SIRT1 being a primary focus. Bioinformatics and Immunoprecipitation mass spectrometry analysis, and immunohistochemistry were employed to further elucidate the downstream target of SIRT1, specifically the YAP-NLRP3 pathway. The degradation mechanisms of YAP-NLRP3 were explored using MG132, chloroquine, cycloheximide, and co-immunoprecipitation. Corresponding rescue experiments were conducted in H9C2 cells for further validation. Results Gyp-XLIX effectively mitigates SIC, reduces cardiac inflammation, and restores cardiac structural, left ventricular functional abnormalities, and oxidative stress balance. Proteomics results showed that Gyp-XLIX binded to SIRT1 and alleviates inflammation and oxidative stress. Whereas, SIRT1 is low expressed and alleviated oxidative stress and NLRP3 inflammasome activation in SIC. Mechanically, Gyp-XLIX binded to SIRT1 improved its stability and promoted the deacetylation and phosphorylation of downstream YAP, which in turn regulated YAP degradation. This process subsequently affects the ubiquitination of NLRP3, downstream of YAP, at the K27 site, leading to its degradation and, consequently, alleviating inflammation and oxidative stress during SIC. Conclusion Gyp-XLIX targets SIRT1 to block YAP-NLRP3 activation and improve SIC, suggesting that Gyp-XLIX is an effective protective agent against SIC and represents a promising therapeutic strategy.
研究领域:
心血管药理学
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分子医学
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炎症生物学
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天然产物研究
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信号转导
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产品关联
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
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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产品关联
DOI
PubMed
高影响因子
JOURNAL OF ANIMAL SCIENCE
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2026
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IF 3.7
Zheng Jikang,Zhao Junyin,Li Minhao,Cheng Yuqin,Fang Xingqiang,Zhao Le,Zhao Yongju
Goat semen cryopreservation generates excessive reactive oxygen species (ROS), which impair post-thaw quality and physiological function. This study investigated the effects of resveratrol (RES) on cryopreserved goat sperm and the underlying signaling pathway. The results showed that supplementation with 150 μM RES significantly improved post-thaw sperm motility, plasma membrane integrity, and acrosome integrity (P < 0.05), enhanced SOD, CAT, and T-AOC activities, and reduced MDA content and sperm deformity rates (P < 0.05), while higher concentration (200 μM) showed no significant improvement compared to control, suggesting a detrimental effect of excessive RES. Furthermore, RES effectively alleviated cryo-induced ultrastructural damage to sperm. Mechanistically, RES activated AMPK signaling, increased AMPK phosphorylation, and upregulated the expression of SIRT1 and FoxO1 proteins. In contrast, the AMPK inhibitor Compound C partially blocked these beneficial effects. These findings indicate that RES improves the quality and antioxidant capacity of cryopreserved goat sperm by activating the AMPK/SIRT1/FoxO1 pathway, suggesting that RES can serve as a promising antioxidant additive for goat semen cryopreservation.
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产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
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2025
·
IF 4.8
Shuzhen Mao,Jiahui Huang,Junyan Li,Fang Sun,Qilian Zhang,Qing Cheng,Wei Zeng,Dongya Lei,Shiyan Wang,Jing Yao
Introduction: Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized by mucosal damage and impaired epithelial barrier function. While glycyl-l-histidyl-l-lysine-copper (GHK-Cu) exhibits known anti-inflammatory properties, its therapeutic mechanisms in UC remain undefined. This study was designed to systematically evaluate the therapeutic potential of GHK-Cu in a dextran sulfate sodium (DSS)-induced murine model of UC, with particular emphasis on elucidating its regulatory effects on the NAD-dependent deacetylase sirtuin-1 (SIRT1)/signal transducer and activator of transcription 3 (STAT3) signaling pathway.Methods: UC was induced in BALB/c mice with 3% DSS for 14 days. The protein expression levels of tight junction associated protein-1 (ZO-1), Occludin, inflammatory factors interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α, SIRT1, STAT3, p-STAT3, and retinoic acid receptor-related orphan receptor gamma t (RORγt) were detected by Western blot. Histopathological changes were evaluated by Hematoxylin and Eosin (H&E) and Alcian blue-periodic acid-Schiff (AB-PAS). Network pharmacology and molecular docking were used to predict the core targets of GHK Cu in the treatment of UC. An in vitro UC model was also established in mouse peritoneal macrophages (MPMs) using lipopolysaccharide (LPS), and a co culture model was constructed using mouse colonic epithelial cells (MCECs) and MPMs to examine the role of GHK Cu in promoting mucosal healing. STAT3 was silenced by gene transfection technology to verify the core role of STAT3 in GHK Cu treatment of UC.Results: GHK-Cu alleviated weight loss, improved the disease activity index (DAI), reduced colonic edema and shortening, attenuated inflammatory damage, increased goblet cell numbers, suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and promoted mucosal repair. Additionally, a co-culture system of MCECs and MPMs revealed that GHK-Cu facilitated MCECs healing, impaired by DSS, by upregulating ZO-1 and Occludin expression. Subsequently, network pharmacology and molecular docking identified SIRT1 as a potential target of GHK-Cu. Results showed that GHK-Cu upregulated SIRT1 protein expression and suppressed the expression of phosphorylated p-STAT3 in colon tissue and MCECs of the co-culture model. Our findings revealed that after transfection with STAT3-targeting siRNA (siSTAT3), the stimulant effect of GHK-Cu on the healing of MCECs and the effect on the protein expression of ZO-1 and Occludin is canceled. Nevertheless, after transfection with siSTAT3, it could inhibit the expression of inflammatory factors in conjunction with GHK-Cu. Furthermore, we found that GHK-Cu could inhibit RORγt expression in the colon tissue of UC mice.Discussion: This study found that GHK-Cu demonstrated significant therapeutic effects in DSS-induced UC in mice. GHK-Cu may promote mucosal healing and enhance tight junction protein expression by regulating the SIRT1/STAT3 pathway. In addition to suppressing p-STAT3 expression, GHK-Cu may utilize additional pathways to inhibit inflammatory factors. Furthermore, GHK-Cu may reduce the number of Th17 cells. In summary, GHK-Cu may treat UC by acting on the SIRT1/STAT3 pathway.
研究领域:
药理学
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免疫学
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分子生物学
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胃肠病学
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产品关联
DOI
PubMed
高影响因子
MACROMOLECULAR BIOSCIENCE
·
2021
·Vol. 22
·期 3
·2100440
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IF 4.979
Rong You,Lu Shi,Surong Chen,Qingpeng Liu,Lingkun Zhang,Liang Yin,Runcai Yang,Yan-Qing Guan
In this research, resveratrol (RSV)-loaded scaffolds have been prepared to control the release of resveratrol and used to delay hepatic stellate cell (HSC) senescence in vitro. The functional carboxyl group–COOH is first introduced to the surface of poly( ε -caprolactone/ d , l -lactide) (P(CL-DLLA)) under the coadministration of ultra-violet (UV) treatment and photo initiator and then resveratrol are conjugated onto the surface of the modified scaffolds through esterification. The characterization of the structure of RSV-AA-P(CL-DLLA) shows that resveratrol has been successfully conjugated onto the modified surface. Cell growth exhibits a higher level of cell viability and much more obvious agglomeration on the surface of the synthetic RSV-AA-P(CL-DLLA). Meanwhile the activity of senescence-associated β -galactosidase (SA- β -gal) and reactive oxygen species (ROS) is downgulated for cells on RSV-AA-P(CL-DLLA), which suggests that cell senescence is delayed on RSV-AA-P(CL-DLLA). And then it is attested that cells have a lower level of p53 but SIRT1 expression is upregulated on RSV-AA-P(CL-DLLA), which might be related to resveratrol release from RSV-AA-P(CL-DLLA). It also suggested cell senescence on RSV-AA-P(CL-DLLA) has been regulated by p53 and the SIRT1 signaling pathway. In all, the present study shows that RSV-AA-P(CL-DLLA) can be successfully prepared to promote cell growth and delay cell senescence and could be used for cell-based therapy in tissue engineering.
研究领域:
生物材料学
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细胞生物学
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组织工程学
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产品关联
DOI
PubMed
高影响因子
Cell Metabolism
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2025
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IF 30.9
Jie Jiang,Yuqing Gao,Jiang Wang,Yan Huang,Rong Yang,Yongxin Zhang,Yuandi Ma,Yingquan Wen,Gongkai Luo,Shurui Zhang,Yutang Cao,Minjun Yu,Qinxue Wang,Shulei Hu,Kanglong Wang,Xiaozhen Guo,Frank J. Gonzalez,Yameng Liu,Hong Liu,Qing Xie,Cen Xie
Metabolic-dysfunction-associated steatohepatitis (MASH) remains a major health challenge. Herein, we identify sphingomyelin phosphodiesterase 3 (SMPD3) as a key driver of hepatic ceramide accumulation through increasing sphingomyelin hydrolysis at the cell membrane. Hepatocyte-specific Smpd3 gene disruption or pharmacological inhibition of SMPD3 alleviates MASH, whereas reintroducing SMPD3 reverses the resolution of MASH. Although healthy livers express low-level SMPD3, lipotoxicity-induced DNA damage suppresses sirtuin 1 (SIRT1), triggering an upregulation of SMPD3 during MASH. This disrupts membrane sphingomyelin-ceramide balance and promotes disease progression by enhancing caveolae-dependent lipid uptake and extracellular vesicle secretion from steatotic hepatocytes to exacerbate inflammation and fibrosis. Consequently, SMPD3 acts as a central hub integrating key MASH hallmarks. Notably, we discovered a bifunctional agent that simultaneously activates SIRT1 and inhibits SMPD3, which shows significant therapeutic potential in MASH treatment. These findings suggest that inhibition of hepatic SMPD3 restores membrane sphingolipid metabolism and holds great promise for developing novel MASH therapies.
研究领域:
生物化学
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肝脏病学
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代谢医学
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产品关联
DOI
PubMed
高影响因子
MOLECULES
·
2019
·Vol. 24
·期 6
·1105
·
IF 3.06
Jiancheng Wang,Cuilin Cheng,Chao Xin,Zhenyu Wang
Fenugreek (Trigonella Foenum-Graecum) seeds flavonoids (FSF) have diverse biological activities, while the antidepressant-like effect of FSF has been seldom explored. The aim of this study was to evaluate the antidepressant-like effect of FSF and to identify the potential molecular mechanisms. LC-MS/MS was used for the determination of FSF. Chronic restraint stress (CRS) was used to establish the animal model of depression. Observation of exploratory behavior in the forced swimming test (FST), tail suspension test (TST) and sucrose preference test (SPT) indicated the stress level. The serum corticosterone (CORT) level was measured. The monoamine neurotransmitters (5-HT, NE and DA) and their metabolites, as well as monoamine oxidase A (MAO-A) enzyme activity in the prefrontal cortex, hippocampus and striatum, were evaluated. The protein expression levels of KLF11, SIRT1, MAO-A were also determined by western blot analysis. The results showed that FSF treatment significantly reversed the CRS-induced behavioral abnormalities, including reduced sucrose preference and increased immobility time. FSF administration markedly restored CRS induced changes in concentrations of serum corticosterone, prefrontal cortex neurotransmitters (NE, 5-HT and DA), hippocampus neurotransmitters (NE, 5-HT and DA) and striatum neurotransmitters (NE). FSF treatment exhibited significant inhibition of MAO-A activity in the prefrontal cortex and hippocampus. FSF also significantly down-regulated the KLF11, SIRT1 and MAO-A protein expression levels in the prefrontal cortex and hippocampus. These findings indicate that FSF could exhibit an antidepressant-like effect by down-regulating the KLF11/SIRT1-MAO-A pathways, inhibiting MAO-A expression and activity, as well as up-regulating monoamine neurotransmitters levels.Keywords:flavonoids;depression;monoamine neurotransmitters;monoamine oxidase A;KLF11;SIRT1
研究领域:
药理学
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神经科学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
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2020
·
IF 1.466
Zhan Wang,Rui Chen,Zheming Xu,Wei Ru,Hongjuan Tian,Fan Yang,Chang Tao
Protection against renal fibrosis is important for the management of obstructive nephropathy. We researched the roles and possible mechanism of miR-155-5p in renal interstitial fibrosis, which may provide a potential endogenous target for renal interstitial fibrosis in obstructive nephropathy. Herein, NRK-49F cells were transfected with miR-155-5p mimic, miR-155-5p inhibitor, SIRT1 plasmid and/or SIRT1 siRNA. The unilateral ureteral obstruction (UUO) model was built with male C57 black mice and administrated with SRT1720 by tail vein injection. Levels of miR-155-5p, SIRT1 and relative proteins (TGF-β1, α-SMA, Collage I and fibronectin) in NRK-49F cells or mice kidney tissues were measured with quantitative reverse transcription polymerase chain reaction or Western blot. The target gene of miR-155-5p was analyzed through TargetScan and dual-luciferase reporter assay. Mice kidney tissue was stained with Masson trichrome. It was found that miR-155-5p overexpression promoted the expressions of fibroblast related proteins expression and inhibited the SIRT1 expression in NRK-49F cells, while miR-155-5p silencing had an opposite effect. SIRT1 can bind with miR-155-5p. MiR-155-5p inhibited the level of SIRT1. Fibroblast related proteins were up-regulated by miR-155-5p and down-regulated by SIRT1 in NRK-49F cells, while the up-regulatory effect of miR-155-5p was reversed by SIRT1. MiR-155-5p expression was up-regulated and SIRT1 expression was down-regulated in the kidney tissue of UUO mice. SRT1720 attenuated the fiber deposition, up-regulated SIRT1 level and down-regulated the levels of fibroblast related proteins in UUO model mice. To conclude, miR-155-5p promotes renal interstitial fibrosis in obstructive nephropathy via inhibiting SIRT1 signaling pathway.
研究领域:
肾病学
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分子生物学
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病理学
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DOI
PubMed
高影响因子
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