Relationship between angiotensin-converting enzyme insertion/deletion gene polymorphism and prostate cancer susceptibility.

BACKGROUND AND OBJECTIVE: Investigations on the relationship between angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism and prostate cancer risk are conflicting. This meta-analysis was conducted to assess the relationship between ACE I/D gene polymorphism and prostate cancer risk. MATERIALS AND METHODS: Reports were identified from PubMed, Cochrane Library, and China Biological Medicine (CBM)-disc (CBM database) on December 30, 2014, and eligible studies were recruited. RESULTS: ACE I/D gene polymorphism was not associated with prostate cancer risk for overall populations in this meta-analysis (D allele: Odds ratio [OR] =1.56, 95% confidence interval [95% CI]: 1.00-2.46, P = 0.05; DD genotype: OR = 1.74, 95% CI: 0.95-3.20, P = 0.07; II genotype: OR = 0.67, 95% CI: 0.39-1.15, P = 0.15). Furthermore, the association of ACE I/D gene polymorphism with colorectal cancer risk was not found for the Caucasians. Interestingly, ACE I/D gene polymorphism was associated with prostate cancer risk for the Asian population and Latino population. CONCLUSIONS: There was an association between ACE I/D gene polymorphism and prostate cancer risk for the Asians and Latino population in this meta-analysis. However, more investigations should be performed to confirm this relationship.

Levels of vitamin D receptor and CYP24A1 in patients with end-stage renal disease.

OBJECTIVE: This study was performed to detect the expression of vitamin D receptor (VDR) and cytochrome P450, family 24, subfamily A, polypeptide 1 (CYP24A1) in 24 end stage renal disease (ESRD) patients and 24 healthy controls. METHOD: In this study, 24 ESRD patients and 24 healthy controls were included. RESULTS: In our study, the levels of VDR in patients with ESRD were reduced when compared with those from healthy controls (5.20±0.32 vs 8.59±1.03; P<0.01). However, the levels of CYP24A1 in ESRD patients were increased than those from healthy controls (50.18±21 vs 7.78±1.31; P<0.01). Correlation analysis showed that VDR levels were negatively correlated with CYP24A1 (r=-0.723; P<0.01). CONCLUSION: VDR levels were reduced and CYP24A1 levels were increased in patients with ESRD, and VDR levels were negatively correlated with CYP24A1.

Potential signal pathway between all-trans retinoic acid and LMX1B in hypoxia-induced renal tubular epithelial cell injury.

All-trans retinoic acid (ATRA), an active metabolite of vitamin A, exerts various effects on physiological processes such as cell growth, differentiation, apoptosis and inflammation. LMX1B, a developmental LIM-homeodomain transcription factor, is widely expressed in vertebrate embryos, and it takes part in the development of diverse structures such as limbs, kidneys, eyes, brains, etc. Renal tubular epithelial cell culture was performed, and mRNA and protein expression of some factors were detected. We recently demonstrated that ATRA up-regulated the LMX1B, and down-regulated the transforming growth factor-ß1, collagen IV and fibronectin in a hypoxia/reoxygenation (H-R) injury system in renal tubular epithelial cells (RTEC). In conclusion, ATRA acts as a positive regulator of LMX1B in H-R RTEC.

GSTM1 Gene Polymorphism is Implicated in Increased Susceptibility to Prostate Cancer in Caucasians and Asians.

Published reports on the relationship between GSTM1 gene polymorphisms and prostate cancer risk are heterogeneous in their conclusions, and the significance of these polymorphisms is still debated. This meta-analysis was performed to attempt to combine comparable studies, thereby increasing sample size and statistical significance in order to obtain a better evaluation of the association between GSTM1 polymorphisms and prostate cancer risk. The association investigations were identified from PubMed, Cochrane Library, and China Biological Medicine Database on March 1, 2014. Forty-three reports were recruited into this meta-analysis that contained data from 6741 patients and 9053 controls. There was a marked association between the GSTM1 null genotype and prostate cancer risk in the overall population (odds ratio = 1.39, 95% confidence interval: 1.21-1.60, P <00001), caucasians (odds ratio = 1.48, 95% confidence interval: 1.23-1.79, P <0001) and Asians (odds ratio = 1.62, 95% confidence interval: 1.16-2.27, P = .005). However, the GSTM1 null genotype was not associated with prostate cancer risk in Africans (odds ratio = 0.77, 95% confidence interval: 0.53-1.13, P = 0.19) and African Americans (odds ratio = 1.00, 95% confidence interval: 0.69-1.45, P = 0.99). In conclusion, GSTM1 null genotype was a risk factor to predict the prostate cancer risk in the overall population, Caucasians, and Asians. Although compelling, limitations inherent to meta-analysis, study design of the individual studies, and most importantly, possible gene-gene and gene-environment interactions, as well as the potential involvement of glutathione S-transferases in multiple cellular processes make drawing definite conclusions difficult.

Is there an association of hepatitis B virus infection with minimal change disease of nephrotic syndrome? A clinical observational report.

The rate of hepatitis B virus (HBV) infection is high in the Chinese population, and the implications of HBV infection are widely recognized, and membranous nephropathy is the most common renal lesion to be associated with HBV infection. Minimal change disease (MCD) is one of the most important histopathological characteristics in patients with nephrotic syndrome. There is no any study to report that HBV infection is associated with the etiology of MCD. Herein, we report four MCD patients with HBV infection and speculate that there is an association of HBV infection with the pathological type of MCD. In this study, we also reported the treatment schedule for these four MCD patients, and found that the anti-virus alone and combination of anti-virus with immunosuppressive agent could obtain a benefit for MCD patients with HBV infection. However, a well-designed study should be performed to confirm this association.

RETRACTED: Role of renin-angiotensin-aldosterone system inhibitors in radiation nephropathy.

The following article has been included in a multiple retraction: Tian-Biao Zhou, Hong-Yan Li, Zong-Pei Jiang, Jia-Fan Zhou, Miao-Fang Huang and Zhi-Yang Zhou Role of renin-angiotensin-aldosterone system inhibitors in radiation nephropathy Journal of Renin-Angiotensin-Aldosterone System ( JRAAS) 1470320314563424, first published 18 December 2014. DOI: 10.1177/1470320314563424 . This article has been retracted at the request of the Editors and the Publisher. After conducting a thorough investigation, SAGE found that the submitting authors of a number of papers published in the JRAAS (listed below) had supplied fabricated contact details for their nominated reviewers. The Editors accepted these papers based on the reports supplied by the individuals using these fake reviewer email accounts. After concluding that the peer-review process was therefore seriously compromised, SAGE and the journal Editors have decided to retract all affected articles. Online-first articles (these articles will not be published in an issue) Wenzhuang Tang, Tian-Biao Zhou and Zongpei Jiang Association of the angiotensinogen M235T gene polymorphism with risk of diabetes mellitus developing into diabetic nephropathy JRAAS 1470320314563426, first published 18 December 2014. DOI: 10.1177/1470320314563426 . Tian-Biao Zhou, Hong-Yan Li, Zong-Pei Jiang, Jia-Fan Zhou, Miao-Fang Huang and Zhi-Yang Zhou Role of renin-angiotensin-aldosterone system inhibitors in radiation nephropathy JRAAS 1470320314563424, first published 18 December 2014. DOI: 10.1177/1470320314563424 . Weiqiang Zhong, Zongpei Jiang and Tian-Biao Zhou Association between the ACE I/D gene polymorphism and T2DN susceptibility: The risk of T2DM developing into T2DN in the Asian population JRAAS1470320314566019, first published 26 January 2015. DOI: 10.1177/1470320314566019 . Tian-Biao Zhou, Xue-Feng Guo, Zongpei Jiang and Hong-Yan Li Relationship between the ACE I/D gene polymorphism and T1DN susceptibility/risk of T1DM developing into T1DN in the Caucasian population JRAAS 1470320314563425, first published 1 February 2015. DOI: 10.1177/1470320314563425 . Chun-Hua Yang and Tian-Biao Zhou Relationship between the angiotensinogen A1166C gene polymorphism and the risk of diabetes mellitus developing into diabetic nephropathy JRAAS 1470320314566221, first published 1 February 2015. DOI: 10.1177/1470320314566221 . Chun-Hua Yang and Tian-Biao Zhou Association of the ACE I/D gene polymorphism with sepsis susceptibility and sepsis progression JRAAS 1470320314568521, first published 3 February 2015. DOI: 10.1177/1470320314568521 . Articles published in an issue Guohui Liu, Tian-Biao Zhou, Zongpei Jiang and Dongwen Zheng Association of ACE I/D gene polymorphism with T2DN susceptibility and the risk of T2DM developing into T2DN in a Caucasian population JRAAS March 2015; 16: 165-171, first published 14 November 2014. DOI: 10.1177/1470320314557849 . Weiqiang Zhong, Zhongliang Huang, Yong Wu, Zongpei Jiang and Tian-Biao Zhou Association of aldosterone synthase ( CYP11B2) gene polymorphism with IgA nephropathy risk and progression of IgA nephropathy JRAAS September 2015; 16: 660-665, first published 20 August 2014. DOI: 10.1177/1470320314524011 .

The potential signaling pathway between peroxisome proliferator-activated receptor gamma and retinoic acid receptor alpha in renal interstitial fibrosis disease.

Peroxisome proliferator-activated receptorγ (PPARγ) can regulate the process of cell apoptosis and is related to the progression of renal disorders. Retinoic acid receptor alpha (RARα) is one of the nuclear receptors involved in a variety of kidney diseases. Renal interstitial fibrosis (RIF) is a common denominator of chronic kidney disease (CKD). This study investigated whether a potential signaling pathway existed between PPARγ and RARα in RIF rats with unilateral ureteral obstruction (UUO). The rats were randomly divided into four groups: a model group subjected to UUO (GU), and three other groups treated with rosiglitazone sodium (GRS), GW9662 and dimethyl sulfoxide (DMSO), n = 40, respectively. Renal tissues were collected two and four weeks after post-surgery. The relevant indicators were detected. In comparison with the GU group, the expressions of PPARγ and RARα (protein and mRNA) were increased in the GRS group, and decreased in the GW9662 group (all p < 0.01). The RIF index, mRNA and protein expression of transforming growth factor-ß1 (TGF-ß1), and the protein expressions of collagen-IV (Col-IV) and fibronectin (FN) in the GRS group were more markedly reduced than those in the GU group; their levels in the GW9662 group were elevated (all p < 0.01). PPARγ or RARα was negatively correlated to the RIF index, TGF-ß1, Col-IV and FN. PPARγ was positively correlated with RARα (all p < 0.01). In conclusion, PPARγ agonist can elevate the expression of PPARγ or RARα in RIF rats. There might be a potential signaling pathway between PPARγ and RARα in RIF disease.

Role of MAPK signal pathways in differentiation process of M2 macrophages induced by high-ambient glucose and TGF-ß1.

Macrophage can be alternatively activated by TGF-ß1, whether high-ambient glucose can enhance the sensitivity of TGF-ß1 and the intracellular mechanisms involved in this process are not fully understood. We examined whether the mitogen-activated protein kinase is involved in the activation of macrophage induced by TGF-ß1 and high-ambient glucose. The expression of arginase-1, CD206 and TGF-ß1 was accessed by Western blot and immunofluorescence in RAW 264.7 cells stimulated with TGF-ß1 and high-ambient glucose. The activation of MAPK pathways in the process was investigated by Western blot. The role of MAPK was assessed using biochemical inhibitors. The protein of arginase-1, CD206 and TGF-ß1 was significantly overexpressed in RAW264.7 cells stimulated by TGF-ß1 and high-ambient glucose. ERK and JNK phosphorylation occurred in 30 min and p38MAPK phosphorylation occurred in 30 min and 24 h after the stimulation. And the expression of arginase-1 and TGF-ß1 was partially blocked by the pretreated ERK biochemical inhibitor (U0126) instead of the JNK inhibitor (SP600125) and p38MAPK inhibitor (SB203580). In conclusion, high-ambient glucose can enhance the sensitivity of TGF-ß1 in RAW264.7 cells, which resulted in overexpression of TGF-ß1 and arginase-1 in macrophages. ERK plays a role in this process.

Roles of miR-497 and its potential signaling pathway in diseases and with vascular endothelial growth factor.

MicroRNA (miRNA) is a class of small endogenous non-coding RNAs that are ∼ 22 nucleotides in length and can have structural, enzymatic and post-transcriptional regulators of gene expression targeting mRNA for translational repression and/or degradation. miR-497 is high on the list of noncoding, small, regulatory RNAs that plays important roles in the pathogenesis of some diseases and takes part in some signaling pathways in some diseases, but many questions await answers. Vascular endothelial growth factor (VEGF) is a notable chemokine that plays critical roles in angiogenesis and vasculogenesis. There might be an association between miRNA-497 and VEGF. This review was performed to sum up the roles of miR-497 and its potential signaling pathway in diseases and with VEGF.

Effect of all-trans retinoic acid treatment on prohibitin and renin-angiotensin-aldosterone system expression in hypoxia-induced renal tubular epithelial cell injury.

BACKGROUND AND OBJECTIVE: All-trans retinoic acid (ATRA) exerts various effects on physiological processes such as cell growth, differentiation, apoptosis and inflammation. Prohibitins (PHB), including prohibitin 1 (PHB1) and prohibitin 2 (PHB2), are evolutionary conserved and pleiotropic proteins implicated in various cellular functions, including proliferation, tumor suppression, apoptosis, transcription, and mitochondrial protein folding. The renin-angiotensin-aldosterone system plays a pivotal role in the regulation of blood pressure and volume homeostasis. All these factors and systems have been implicated in renal interstitial fibrosis. Therefore, the objective of this study was to investigate the effect of ATRA treatment on the renin-angiotensin-aldosterone system and expression of prohibitins to further understand its role in the processes leading to renal interstitial fibrosis. METHODS: The hypoxic and oxidative stress conditions in obstructive renal disease were simulated in a hypoxia/reoxygenation model with renal tubular epithelial cells (RTEC) as a model system. Subsequently, the effect of ATRA on mRNA and protein expression levels was determined and correlations were established between factors involved in the renin-angiotensin-aldosterone system, the prohibitins, cellular redox status, renal interstitial fibrosis and ATRA treatment. RESULTS: Correlation analysis showed that both PHB1 and PHB2 protein levels were negatively correlated with angiotensin I, ACE1, angiotensin II, TGF-ß1, Col-IV, FN, ROS, and MDA (PHB1: r = -0.792, -0.834, -0.805, -0.795, -0.778, -0.798, -0.751, -0.682; PHB2: r = -0.872, -0.799, -0.838, -0.773, -0.769, -0.841, -0.794, -0.826; each p < 0.05), but positively correlated with ACE2, SOD, and GSH (PHB1: r = 0.796, 0.879, 0.824; PHB2: r = 0.785, 0.914, 0.849; each p < 0.05). ACE1 was positively correlated with angiotensin I, angiotensin II, TGF-ß1, Col-IV, FN, ROS, and MDA, and negatively correlated with ACE2, SOD, and GSH (each p < 0.05). ACE2 was negatively correlated with ACE1, angiotensin I, angiotensin II, TGF-ß1, Col-IV, FN, ROS, and MDA, and positively correlated with SOD and GSH (each p < 0.05). CONCLUSION: The results suggest that ATRA acts as a positive regulator of PHB1, PHB2 and ACE2, and as a negative regulator of ACE1, angiotensin I, and angiotensin II in a RTEC model system under hypoxia/reoxygenation conditions.

GSTT1 polymorphism and the risk of developing prostate cancer.

A possible association between glutathione S-transferase theta 1 gene (GSTT1) polymorphism and the risk of developing prostate cancer is currently hotly debated, but evidence from various epidemiologic studies remains unclear. This investigation was performed to assess whether an association between GSTT1 polymorphism and prostate cancer risk exists by using meta-analysis to combine comparable studies, thereby increasing sample size and statistical significance, as well as to identify patterns in various studies. The association reports were identified from the PubMed database and the Cochrane Library on March 1, 2013, and data from eligible studies (from 1999-2012) were synthesized. Thirty-eight reports were included in this meta-analysis on the association of the null genotype of GSTT1 with prostate cancer risk. No solid association between the GSTT1 null genotype and prostate cancer risk could be established for the overall population (odds ratio = 1.11, 95% confidence interval: 0.97, 1.27; P = 0.13). However, the GSTT1 null genotype was distinctly associated with prostate cancer risk in Caucasians (odds ratio = 1.24, 95% confidence interval: 1.03, 1.48, P = 0.02). In conclusion, the GSTT1 null genotype is associated with prostate cancer risk in Caucasians, but not in the overall population.

Distribution of pathological finding in the children with nephrotic syndrome from Guangxi.

To identify the variations in pediatric renal biopsy pathology and clinicopathological features in Guangxi, China, in the past ten years, we studied retrospectively the kidney biopsies performed to evaluate the primary nephrotic syndrome (PNS) in 218 children at two main medical centers in Guangxi from January 1999 to January 2009. The major pathological finding was mesangial proliferative glomerulonephritis (48.2%), focal segmental glomerulosclerosis (16.5%), immunoglobulin A nephropathy (13.3%) and minimal change disease (11.0%). Patients with different pathological types yielded different response rates to glucocorticoids (P <0.001). There were statistical significant differences between prognosis for the different pathological types (P <0.05). The pathological characteristics of PNS in children were diverse and significant for guiding the grade of glucocorticoid response and predicting the prognosis of the PNS disease.

Role of high mobility group box 1 and its signaling pathways in renal diseases.

The high mobility group box 1 (HMGB1) protein, a member of the high mobility group nuclear protein family and an endogenous ligand for TLR2/4 and RAGE (receptor for advanced glycation end products), is one of the most evolutionarily conserved proteins and it has recently emerged as an extracellular signaling factor with key roles in cell differentiation, proliferation and disease pathogenesis. The present data indicate that HMGB1 is one of most important proinflammatory cytokines, and plays an important role in renal diseases. The literatures were searched extensively and this review was performed to sum up the role of HMGB1 in renal diseases.

Association of prohibitin-1 and 2 with oxidative stress in rats with renal interstitial fibrosis.

Prohibitins PHB1 and PHB2 are evolutionary conserved and pleiotropic proteins, which have been shown to be important factors in various cellular functions, including proliferation, tumour suppression, apoptosis, transcription, and mitochondrial protein folding. Recently, we demonstrated that down-regulation promoted renal interstitial fibrosis (RIF) in ureteral obstructed rats. Furthermore, the hypoxic conditions and oxidative stress have been implicated in obstruction-mediated renal disease. This study was performed to explore the association of PHBs with oxidative stress in a rat model of RIF. PHBs, the pro-fibrotic transforming growth factor-ß1 (TGF-ß1), and the extracellular matrix proteins collagen-IV (Col-IV) and fibronectin (FN) were evaluated, as were markers of oxidative stress [total reactive oxygen species (ROS), malondialdehyde (MDA)] and antioxidative capacity (superoxide dismutase, glutathione), and apoptosis. Our results showed a progressive increase in oxidative stress and concomitant decrease in antioxidants over a period of 4 weeks ureteral obstruction. Concomitantly, profibrotic components increased and PHB expression decreased. Overall, both PHBs were negatively correlated with the extent of observed fibrosis, TGF-ß1, Col-IV, FN, ROS, MDA, and apoptosis.

Role of miR-107 and its signaling pathways in diseases.

MicroRNAs exert their biologic effects by targeting specific mRNAs for degradation or translational inhibition. MicroRNA-mediated regulation is complex, potentially affecting expression of the host gene, related enzymes within the same pathway or apparently distinct targets. miR-107 is found to be implicated in the pathogenesis of some diseases. This review was performed to sum up the role of miR-107 and its signaling pathways in renal diseases.

The potential signal pathway between PAX2 and CD2AP in the renal interstitial fibrosis disease.

Paired box gene 2 (PAX2) can regulate tissue development and cellular differentiation, and it is associated with renal diseases. CD2-associated protein (CD2AP) is an adaptor protein involving in a variety of physiological and disease processes. Renal interstitial fibrosis (RIF) is a hallmark of common progressive chronic diseases which lead to renal failure. This study was performed to investigate whether there was a potential signal pathway between PAX2 and CD2AP in RIF rats induced by unilateral ureteral obstruction (UUO). Eighty Wistar male rats were divided into two groups randomly: sham operation group (SHO) and model group subjected to UUO (GU), n = 40. The model was established by left ureteral ligation. Renal tissues were collected at 14 d and 28 d after surgery. RIF index, cell apoptosis index, protein expression of PAX2, CD2AP, transforming growth factor-ßl (TGF-ß1), collagen-IV (Col-IV), fibronectin (FN) in renal interstitium and renal tissue, and mRNA expression of PAX2, CD2AP, and TGF-ß1 in renal tissue were detected. Compared with that in the SHO group, the PAX2 and CD2AP expressions (mRNA and protein) were significantly increased (p < 0.01). Protein expressions of TGF-ß1, Col-IV, and FN, and RIF index or cell apoptosis index in the GU group were markedly elevated than those in the SHO group (all p < 0.01). PAX2 or CD2AP was positively correlated with TGF-ß1, Col-IV, and FN, and RIF index or cell apoptosis index (all p < 0.05). Furthermore, PAX2 was positively correlated with CD2AP (p < 0.05). In conclusion, the expression of PAX2 or CD2AP was increased in RIF rats, and PAX2 was positively correlated with CD2AP. There might be a potential signaling pathway between PAX2 and CD2AP in RIF disease. Further research is needed to determine the association in RIF disease.

LIM homeobox transcription factor 1B is associated with pro-fibrotic components and apoptosis in hypoxia/reoxygenation renal tubular epithelial cells.

LIM homeobox transcription factor 1B (LMX1B) is a transcription factor of the LIM-homeodomain type, which plays an important role in foetal development during formation of the extremities, kidneys, eyes, and the brain. Furthermore, LMX1B has been implicated in nail-patella syndrome, which is predominantly characterized by malformation of limbs and nails, and in 30 % of patients, nephropathy, including renal fibrosis, is observed. Since no reports were available that studied the link between LMX1B expression and pro-fibrotic components and apoptosis in hypoxic renal tubular epithelial cells (RTEC), we explored if LMX1B was associated with extracellular matrix components, profibrotic factors, and apoptosis induced by hypoxia/reoxygenation (H-R). In this cell system under hypoxic conditions, when the expression of LMX1B was inhibited in H-R RTEC, the expression of transforming growth factor-ßl, collagen-III, fibronectin, cleaved caspase-3, and cell apoptosis rate was increased. Consequently, overexpression of LMX1B was associated with reduced cell apoptosis, whilst downregulation of LMX1B was associated with increased cell apoptosis in H-R RTEC.

Prohibitin attenuates oxidative stress and extracellular matrix accumulation in renal interstitial fibrosis disease.

Prohibitin is an evolutionary conserved and pleiotropic protein that has been implicated in various cellular functions, including proliferation, tumour suppression, apoptosis, transcription, and mitochondrial protein folding. Both prohibitin over- and under-expression have been implicated in various diseases and cell types. We recently demonstrated that prohibitin down-regulation results in increased renal interstitial fibrosis (RIF). Here we investigated the role of oxidative stress and prohibitin expression in RIF in unilateral ureteral obstructed rats. Lentivirus-based delivery vectors were used to knockdown or over-express prohibitin. Our results show that increased prohibitin expression was negatively correlated with the RIF index, reactive oxygen species, malon dialdehyde, transforming growth factor ß1, collagen IV, fibronectin, and cell apoptosis index. In conclusion, we postulate that prohibitin acts as a positive regulator of mechanisms that counteract oxidative stress and extracellular matrix accumulation and therefore has an antioxidative effect.

Prohibitin is associated with antioxidative protection in hypoxia/reoxygenation-induced renal tubular epithelial cell injury.

Prohibitin is an evolutionary conserved and pleiotropic protein that has been implicated in various cellular functions, including proliferation, tumour suppression, apoptosis, transcription, and mitochondrial protein folding. We recently demonstrated that prohibitin downregulation results in increased renal interstitial fibrosis. Here we investigated the role of oxidative stress and prohibitin expression in a hypoxia/reoxygenation injury system in renal tubular epithelial cells with lentivirus-based delivery vectors to knockdown or overexpress prohibitin. Our results show that increased prohibitin expression was negatively correlated with reactive oxygen species, malon dialdehyde, transforming-growth-factor-ß1, collagen-IV, fibronectin, and apoptosis (r = -0.895, -0.764, -0.798, -0.826, -0.817, -0.735; each P < 0.01), but positively correlated with superoxide dismutase, glutathione and mitochondrial membrane potential (r = 0.807, 0.815, 0.739; each P < 0.01). We postulate that prohibitin acts as a positive regulator of mechanisms that counteract oxidative stress and extracellular matrix accumulation and therefore has an antioxidative effect.

Signaling pathways of apoE and its role of gene expression in glomerulus diseases.

The roles of apolipoprotein E (apoE) in regulating plasma lipids and lipoproteins levels have been investigated for over several decades. However, in different tissues/cells, the role of apoE was different, such as that it was a risk factor for cancer, but some reports stated that apoE was a protective factor for renal diseases. At the moment, most of the studies find that apoE not only acts as a ligand for metabolism of lipids, but also plays as a factor to regulate lots of signaling pathways. There was rare review to sum up the signaling pathways for apoE, and there was also rare review to widely review the gene expression of apoE in glomerulus diseases. This review was performed to provide a relatively complete signaling pathways flowchart for apoE to the investigators who were interested in the roles of apoE in the pathogenesis of glomerulus diseases. In the past decades, some studies were also performed to explore the association of apoE gene expression with the risk of glomerulus diseases. However, the role of apoE in the pathogenesis of glomerulus diseases was controversial. Here, the signal transduction pathways of apoE and its role of gene expression in the pathogenesis of glomerulus diseases were reviewed.