Background The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes b...Background The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells. Recently more attention has been paid to the effect of autophagy in type 2 diabetes. The regulatory pathway of autophagy in controlling pancreatic beta cells is still not clear. The aim of our study was to evaluate whether liraglutide can inhibit apoptosis and modulate autophagy in vitro in insulinoma cells （INS-1 cells）. Methods INS-1 cells were incubated for 24 hours in the presence or absence of high levels of glucose, liraglutide （a long-acting human glucagon-like peptide-1 analogue）, or 3-methyadenine （3-MA）. Cell viability was measured using the Cell Counting Kit-8 （CCK8） viability assay. Autophagy of INS-1 cells was tested by monodansylcadaverine （MDC） staining, an autophagy fluorescent compound used for the labeling of autophagic vacuoles, and by Western blotting of microtubule-associated protein I light chain 3 （LC3）, a biochemical markers of autophagic initiation. Results The viability of INS-1 cells was reduced after treatment with high levels of glucose. The viability of INS-1 cells was reduced and apoptosis was increased when autophagy was inhibited. The viability of INS-1 cells was significantly increased by adding liraglutide to supplement high glucose level medium compared with the cells treated with high glucose levels alone. Conclusions Apoptosis and autophagy were increased in rat INS-1 cells when treated with high level of glucose, and the viability of INS-1 cells was significantly reduced by inhibiting autophagy. Liraglutide protected INS-1 cells from high glucose level-induced apoptosis that is accompanied by a significant increase展开更多
Background:Abnormal lipids are strong predictors of cardiovascular disease in type 1 diabetes mellitus(T1DM)and type 2 diabetes mellitus(T2DM).However,the potential associations of insulin resistance(IR)and beta-cell ...Background:Abnormal lipids are strong predictors of cardiovascular disease in type 1 diabetes mellitus(T1DM)and type 2 diabetes mellitus(T2DM).However,the potential associations of insulin resistance(IR)and beta-cell function(BCF)with abnormal lipids in newly diagnosed T1DM or T2DM patients are not fully understood.Methods:A cross-sectional survey of 15,928 participants was conducted.Homeostasis model assessment and postprandial C-peptide levels were used to estimate IR and BCF.A restricted cubic spline(RCS)nested in binary logistic regression was used to examine the associations of IR and BCF with abnormal lipids.Results:High triglyceride(TG),low high-density lipoprotein cholesterol,and high low-density lipoprotein cholesterol(LDL-C)accounted for 49.7%,47.8%,and 59.2%of the participants,respectively.In multivariable analysis,high IR was associated with an increased risk of high TGs(P for trend<0.001)in T1DM and is associated with an elevated risk of high TG and low HDL-C(all P for trend<0.01)in T2DM.Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.Conclusion:High IR had different associations with the risk of dyslipidemia in newly diagnosed T1DM and T2DM patients,suggesting that early treatment that improves IR may benefit abnormal lipid metabolism.展开更多
BACKGROUND Uncontrolled type 2 diabetes mellitus(T2DM)may lead to microvascular complications(nephropathy,retinopathy,and neuropathy)and cardiovascular diseases.The beta-glucan content in grains has the potential to i...BACKGROUND Uncontrolled type 2 diabetes mellitus(T2DM)may lead to microvascular complications(nephropathy,retinopathy,and neuropathy)and cardiovascular diseases.The beta-glucan content in grains has the potential to improve insulin sensitivity,lowering postprandial glucose response and reducing inflammation degrees.A proper combination of grains not only satisfies human body’s need,but also provides essential and reasonable nutritional contents.However,no trial has been conducted to evaluate the roles of multigrain in T2DM.AIM To determine the efficacy of multigrain supplementation among T2DM patients.METHODS From October 2020 to June 2021,a total of 50 adults living with T2DM,who were receiving standard diabetes care at Day Care Clinic,were randomized into either a supplementation group or a control group.The supplementation group received twice daily 30 g multigrain supplement(equivalent to 3.4 g beta-glucan)with standard medication for 12 wk,while the control group was prescribed with standard medication.Parameters such as glycemic control(HbA1c,FPG,and HOMO-IR),cardiometabolic profile(lipid profile,renal function test,and liver function test),oxidative stress status,nutritional status,and quality of life(QoL)were assessed at two time points:Baseline and the end of the treatment period(week 12).RESULTS The primary outcomes were the mean difference of glycated haemoglobin(%),fasting plasma glucose,and serum insulin as intervention effects.Secondary outcomes included the measurement of cardiometabolic profile,antioxidative and oxidative stress status,nutritional status indices,and QoL.Tertiary outcomes involved the determination of safety and tolerability,and supplementation compliance.CONCLUSION The present clinical trial will reveal the effectiveness of multigrain supplementation among T2DM patients for the improvement of diabetes management.展开更多
The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may...The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.展开更多
Diabetes is an age-related disease,most of which is type 2 diabetes,and islet β cell dysfunction and insulin resistance are the main mechanisms of type 2 diabetes.Recent studies have revealed that autophagy plays an ...Diabetes is an age-related disease,most of which is type 2 diabetes,and islet β cell dysfunction and insulin resistance are the main mechanisms of type 2 diabetes.Recent studies have revealed that autophagy plays an important role in maintaining the structure and func-tion of islet beta cells and inhibiting insulin resistance and apoptosis induced by oxidative stress.In this review,we discussed the positive and negative effects of autophagy and its dysfunction on type 2 diabetes mellitus,which is the so-called double-edged sword,analysed its possible mechanism,and identifed possible research hot spots.展开更多
Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relations...Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U＋/DCX＋double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats.展开更多
Background:In Type 1 diabetes,the insulin-producingβ-cells within the pancreatic islets of Langerhans are destroyed.We showed previously that immunotherapy with Bacillus Calmette-Guerin(BCG)or complete Freund’s adju...Background:In Type 1 diabetes,the insulin-producingβ-cells within the pancreatic islets of Langerhans are destroyed.We showed previously that immunotherapy with Bacillus Calmette-Guerin(BCG)or complete Freund’s adjuvant(CFA)of non-obese diabetic(NOD)mice can prevent disease process and pancreaticβ-cell loss.This was associated with increased islet Regenerating(Reg)genes expression,and elevated IL-22-producing Th17 T-cells in the pancreas.Results:We hypothesized that IL-22 was responsible for the increased Reg gene expression in the pancreas.We therefore quantified the Reg1,Reg2,and Reg3δ(INGAP)mRNA expression in isolated pre-diabetic NOD islets treated with IL-22.We measured IL-22,and IL-22 receptor(R)-αmRNA expression in the pancreas and spleen of pre-diabetic and diabetic NOD mice.Our results showed:1)Reg1 and Reg2 mRNA abundance to be significantly increased in IL-22-treated islets in vitro;2)IL-22 mRNA expression in the pre-diabetic mouse pancreas increased with time following CFA treatment;3)a reduced expression of IL-22Rαfollowing CFA treatment;4)a down-regulation in Reg1 and Reg2 mRNA expression in the pancreas of pre-diabetic mice injected with an IL-22 neutralizing antibody;and 5)an increased isletβ-cell DNA synthesis in vitro in the presence of IL-22.Conclusions:We conclude that IL-22 may contribute to the regeneration ofβ-cells by up-regulating Regenerating Reg1 and Reg2 genes in the islets.展开更多
Objective Ubiquitin-specific protease 4(USP4)facilitates the development of transforming growth factor-beta 1(TGF-β1)-induced epithelial-mesenchymal transition(EMT)in various cancer cells.Moreover,EMT of renal tubula...Objective Ubiquitin-specific protease 4(USP4)facilitates the development of transforming growth factor-beta 1(TGF-β1)-induced epithelial-mesenchymal transition(EMT)in various cancer cells.Moreover,EMT of renal tubular epithelial cells(RTECs)is required for the progression of renal interstitial fibrosis.However,the role of USP4 in EMT of RTECs remains unknown.The present study aimed to explore the effect of USP4 on the EMT of RTECs as well as the involved mechanism.Methods In established unilateral ureteral obstruction(UUO)rats and NRK-52E cells,immunohistochemistry and Western blot assays were performed.Results USP4 expression was increased significantly with obstruction time.In NRK-52E cells stimulated by TGF-β1,USP4 expression was increased in a time-dependent manner.In addition,USP4 silencing with specific siRNA indicated that USP4 protein was suppressed effectively.Meanwhile,USP4 siRNA treatment restored E-cadherin and weakened alpha smooth muscle actin(α-SMA)expression,indicating that USP4 may promote EMT.After treatment with USP4 siRNA and TGF-β1 for 24 h,the expression of TGF-β1 receptor type I(TβRI)was decreased.Conclusion USP4 promotes the EMT of RTECs through upregulating TβRI,thereby facilitating renal interstitial fibrosis.These findings may provide a potential target of USP4 in the treatment of renal fibrosis.展开更多
Endometriosis is a common benign gynecological disorder with an enigmatic etiology and pathogenesis.It affects approximately 10%women of reproductive age.Although its etiology and pathogenesis remain poorly understood...Endometriosis is a common benign gynecological disorder with an enigmatic etiology and pathogenesis.It affects approximately 10%women of reproductive age.Although its etiology and pathogenesis remain poorly understood,it is characterized by the elevated local production of estrogen in the endometriotic tissues.In this paper,we review the mechanisms of estrogen biosynthesis and its regulation in endometriosis.展开更多
基金The study was supported by the grants from the Natural Science Foundation of Heilongjiang Province （No. 200940）, the Science Foundation of the Education Department of Heilongjiang Province （No. 11591157）, and the Science Foundation of the Health Department of Heilongjiang Province （No. 2012-540）.
文摘Background The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells. Recently more attention has been paid to the effect of autophagy in type 2 diabetes. The regulatory pathway of autophagy in controlling pancreatic beta cells is still not clear. The aim of our study was to evaluate whether liraglutide can inhibit apoptosis and modulate autophagy in vitro in insulinoma cells （INS-1 cells）. Methods INS-1 cells were incubated for 24 hours in the presence or absence of high levels of glucose, liraglutide （a long-acting human glucagon-like peptide-1 analogue）, or 3-methyadenine （3-MA）. Cell viability was measured using the Cell Counting Kit-8 （CCK8） viability assay. Autophagy of INS-1 cells was tested by monodansylcadaverine （MDC） staining, an autophagy fluorescent compound used for the labeling of autophagic vacuoles, and by Western blotting of microtubule-associated protein I light chain 3 （LC3）, a biochemical markers of autophagic initiation. Results The viability of INS-1 cells was reduced after treatment with high levels of glucose. The viability of INS-1 cells was reduced and apoptosis was increased when autophagy was inhibited. The viability of INS-1 cells was significantly increased by adding liraglutide to supplement high glucose level medium compared with the cells treated with high glucose levels alone. Conclusions Apoptosis and autophagy were increased in rat INS-1 cells when treated with high level of glucose, and the viability of INS-1 cells was significantly reduced by inhibiting autophagy. Liraglutide protected INS-1 cells from high glucose level-induced apoptosis that is accompanied by a significant increase
基金National Science and Technology Infrastructure Program(Nos. 2013BAI09B12, 2015BAI12B13)National Key R&D Program of China(Nos. 2016YFC1305000, 2017YFC1309604)
文摘Background:Abnormal lipids are strong predictors of cardiovascular disease in type 1 diabetes mellitus(T1DM)and type 2 diabetes mellitus(T2DM).However,the potential associations of insulin resistance(IR)and beta-cell function(BCF)with abnormal lipids in newly diagnosed T1DM or T2DM patients are not fully understood.Methods:A cross-sectional survey of 15,928 participants was conducted.Homeostasis model assessment and postprandial C-peptide levels were used to estimate IR and BCF.A restricted cubic spline(RCS)nested in binary logistic regression was used to examine the associations of IR and BCF with abnormal lipids.Results:High triglyceride(TG),low high-density lipoprotein cholesterol,and high low-density lipoprotein cholesterol(LDL-C)accounted for 49.7%,47.8%,and 59.2%of the participants,respectively.In multivariable analysis,high IR was associated with an increased risk of high TGs(P for trend<0.001)in T1DM and is associated with an elevated risk of high TG and low HDL-C(all P for trend<0.01)in T2DM.Low BCF was not associated with risks of dyslipidemia in patients with T1DM or T2DM after adjustment for potential confounders.Conclusion:High IR had different associations with the risk of dyslipidemia in newly diagnosed T1DM and T2DM patients,suggesting that early treatment that improves IR may benefit abnormal lipid metabolism.
文摘BACKGROUND Uncontrolled type 2 diabetes mellitus(T2DM)may lead to microvascular complications(nephropathy,retinopathy,and neuropathy)and cardiovascular diseases.The beta-glucan content in grains has the potential to improve insulin sensitivity,lowering postprandial glucose response and reducing inflammation degrees.A proper combination of grains not only satisfies human body’s need,but also provides essential and reasonable nutritional contents.However,no trial has been conducted to evaluate the roles of multigrain in T2DM.AIM To determine the efficacy of multigrain supplementation among T2DM patients.METHODS From October 2020 to June 2021,a total of 50 adults living with T2DM,who were receiving standard diabetes care at Day Care Clinic,were randomized into either a supplementation group or a control group.The supplementation group received twice daily 30 g multigrain supplement(equivalent to 3.4 g beta-glucan)with standard medication for 12 wk,while the control group was prescribed with standard medication.Parameters such as glycemic control(HbA1c,FPG,and HOMO-IR),cardiometabolic profile(lipid profile,renal function test,and liver function test),oxidative stress status,nutritional status,and quality of life(QoL)were assessed at two time points:Baseline and the end of the treatment period(week 12).RESULTS The primary outcomes were the mean difference of glycated haemoglobin(%),fasting plasma glucose,and serum insulin as intervention effects.Secondary outcomes included the measurement of cardiometabolic profile,antioxidative and oxidative stress status,nutritional status indices,and QoL.Tertiary outcomes involved the determination of safety and tolerability,and supplementation compliance.CONCLUSION The present clinical trial will reveal the effectiveness of multigrain supplementation among T2DM patients for the improvement of diabetes management.
基金supported by 1RO1EY032959-01,NIH1R15GM124654-01 from NIHSchuellein Chair Endowment Fund and STEM Catalyst Grant and start-up support from the University of Dayton(to AS,MKS is Co-PI on NIH RO1 and Co-I on NIH R15)。
文摘The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.
基金This work was supported by grants from the National Nat-ural Science Foundation of China(grant number 81370885)Research Institute performance incentive and guidance project of Chongqing Science and Technology Bureau(grant number cstc2019jxjl130006)+1 种基金General program of Natural Science Foundation of Chongqing Science and Technology Bureau(grant number cstc2019jcyj-msxm0827)2019 Merck Diabetes Research Fund(grant number g-x-2019-056).
文摘Diabetes is an age-related disease,most of which is type 2 diabetes,and islet β cell dysfunction and insulin resistance are the main mechanisms of type 2 diabetes.Recent studies have revealed that autophagy plays an important role in maintaining the structure and func-tion of islet beta cells and inhibiting insulin resistance and apoptosis induced by oxidative stress.In this review,we discussed the positive and negative effects of autophagy and its dysfunction on type 2 diabetes mellitus,which is the so-called double-edged sword,analysed its possible mechanism,and identifed possible research hot spots.
基金partly supported by the National Natural Science Foundation of China,No.81370448,81570725
文摘Sensitive smell discrimination is based on structural plasticity of the olfactory bulb,which depends on migration and integration of newborn neurons from the subventricular zone.In this study,we examined the relationship between neural stem cell status in the subventricular zone and olfactory function in rats with diabetes mellitus.Streptozotocin was injected through the femoral vein to induce type 1 diabetes mellitus in Sprague-Dawley rats.Two months after injection,olfactory sensitivity was decreased in diabetic rats.Meanwhile,the number of Brd U-positive and Brd U＋/DCX＋double-labeled cells was lower in the subventricular zone of diabetic rats compared with agematched normal rats.Western blot results revealed downregulated expression of insulin receptorβ,phosphorylated glycogen synthase kinase 3β,and β-catenin in the subventricular zone of diabetic rats.Altogether,these results indicate that diabetes mellitus causes insulin deficiency,which negatively regulates glycogen synthase kinase 3β and enhances β-catenin degradation,with these changes inhibiting neural stem cell proliferation.Further,these signaling pathways affect proliferation and differentiation of neural stem cells in the subventricular zone.Dysfunction of subventricular zone neural stem cells causes a decline in olfactory bulb structural plasticity and impairs olfactory sensitivity in diabetic rats.
基金We thank Ms.Brenda Strutt and Jessica Hill for technical help and Dr.Margery Ma from Pfizer,Cambridge,MA for anti-IL-22 antibody.We also thank Dr.Kathleen Hill,Dr.Alexander Timoshenko and Morgan Kleiber for assistance in experimental design and interpretation of the data.This work was supported by grants from the Canadian Institutes of Health Research(CIHR).
文摘Background:In Type 1 diabetes,the insulin-producingβ-cells within the pancreatic islets of Langerhans are destroyed.We showed previously that immunotherapy with Bacillus Calmette-Guerin(BCG)or complete Freund’s adjuvant(CFA)of non-obese diabetic(NOD)mice can prevent disease process and pancreaticβ-cell loss.This was associated with increased islet Regenerating(Reg)genes expression,and elevated IL-22-producing Th17 T-cells in the pancreas.Results:We hypothesized that IL-22 was responsible for the increased Reg gene expression in the pancreas.We therefore quantified the Reg1,Reg2,and Reg3δ(INGAP)mRNA expression in isolated pre-diabetic NOD islets treated with IL-22.We measured IL-22,and IL-22 receptor(R)-αmRNA expression in the pancreas and spleen of pre-diabetic and diabetic NOD mice.Our results showed:1)Reg1 and Reg2 mRNA abundance to be significantly increased in IL-22-treated islets in vitro;2)IL-22 mRNA expression in the pre-diabetic mouse pancreas increased with time following CFA treatment;3)a reduced expression of IL-22Rαfollowing CFA treatment;4)a down-regulation in Reg1 and Reg2 mRNA expression in the pancreas of pre-diabetic mice injected with an IL-22 neutralizing antibody;and 5)an increased isletβ-cell DNA synthesis in vitro in the presence of IL-22.Conclusions:We conclude that IL-22 may contribute to the regeneration ofβ-cells by up-regulating Regenerating Reg1 and Reg2 genes in the islets.
文摘Objective Ubiquitin-specific protease 4(USP4)facilitates the development of transforming growth factor-beta 1(TGF-β1)-induced epithelial-mesenchymal transition(EMT)in various cancer cells.Moreover,EMT of renal tubular epithelial cells(RTECs)is required for the progression of renal interstitial fibrosis.However,the role of USP4 in EMT of RTECs remains unknown.The present study aimed to explore the effect of USP4 on the EMT of RTECs as well as the involved mechanism.Methods In established unilateral ureteral obstruction(UUO)rats and NRK-52E cells,immunohistochemistry and Western blot assays were performed.Results USP4 expression was increased significantly with obstruction time.In NRK-52E cells stimulated by TGF-β1,USP4 expression was increased in a time-dependent manner.In addition,USP4 silencing with specific siRNA indicated that USP4 protein was suppressed effectively.Meanwhile,USP4 siRNA treatment restored E-cadherin and weakened alpha smooth muscle actin(α-SMA)expression,indicating that USP4 may promote EMT.After treatment with USP4 siRNA and TGF-β1 for 24 h,the expression of TGF-β1 receptor type I(TβRI)was decreased.Conclusion USP4 promotes the EMT of RTECs through upregulating TβRI,thereby facilitating renal interstitial fibrosis.These findings may provide a potential target of USP4 in the treatment of renal fibrosis.
基金supported in part by grants 81471434(SWG),81530040(SWG),81370695(XSL),and 81671436(XSL)the National Natural Science Foundation of China.
文摘Endometriosis is a common benign gynecological disorder with an enigmatic etiology and pathogenesis.It affects approximately 10%women of reproductive age.Although its etiology and pathogenesis remain poorly understood,it is characterized by the elevated local production of estrogen in the endometriotic tissues.In this paper,we review the mechanisms of estrogen biosynthesis and its regulation in endometriosis.
