Matches in SemOpenAlex for { <https://semopenalex.org/work/W4289755521> ?p ?o ?g. }
- W4289755521 endingPage "47.e3" @default.
- W4289755521 startingPage "36" @default.
- W4289755521 abstract "Objective The contribution of genetic factors to the presence of an overactive bladder is recognized. This study aimed to (1) assemble and synthesize available data from studies assessing differential gene expression in patients with overactive bladder vs controls without overactive bladder and (2) determine possible correlations and functional pathways between genes. Data Sources We searched PubMed, Ovid or Medline, and Wiley Cochrane Central Register of Controlled Trials databases between January 1, 2000, and December 15, 2021. Study Eligibility Criteria Studies were included if gene expression was detected and quantified using molecular approaches performed on human bladder tissue specimens directly and excluded if the gene expression analysis was carried out from blood and urine specimens alone. Methods A systematic review was completed to identify publications that reported differently expressed gene candidates among patients with overactive bladder vs healthy individuals. Gene networking connections and pathway analysis were performed employing Metascape software, where inputs were identified from our systematic review of differentially expressed genes in overactive bladder. Results A total of 9 studies were included in the final analysis and 11 genes were identified as being up-regulated (purinergic receptor P2X 2 [P2RX2], smoothelin [SMTN], growth-associated protein 43 [GAP43], transient receptor potential cation channel subfamily M member 8 [TRPM8], cadherin 11 [CDH1], gap junction protein gamma 1 [GJC1], cholinergic receptor muscarinic 2 [CHRM2], cholinergic receptor muscarinic 3 [CHRM3], and transient receptor potential cation channel subfamily V member 4 [TRPV4]) or down-regulated (purinergic receptor P2X 2 [P2RX3] and purinergic receptor P2X 5 [P2RX5]) in patients with overactive bladder. Gene network analysis showed that genes are involved in chemical synaptic transmission, smooth muscle contraction, blood circulation, and response to temperature stimulus. Network analysis demonstrated a significant genetic interaction between TRPV4, TRPM8, P2RX3, and PR2X2 genes. Conclusion Outcomes of this systematic review highlighted potential biomarkers for treatment efficacy and have laid the groundwork for developing future gene therapies for overactive bladder in clinical settings. The contribution of genetic factors to the presence of an overactive bladder is recognized. This study aimed to (1) assemble and synthesize available data from studies assessing differential gene expression in patients with overactive bladder vs controls without overactive bladder and (2) determine possible correlations and functional pathways between genes. We searched PubMed, Ovid or Medline, and Wiley Cochrane Central Register of Controlled Trials databases between January 1, 2000, and December 15, 2021. Studies were included if gene expression was detected and quantified using molecular approaches performed on human bladder tissue specimens directly and excluded if the gene expression analysis was carried out from blood and urine specimens alone. A systematic review was completed to identify publications that reported differently expressed gene candidates among patients with overactive bladder vs healthy individuals. Gene networking connections and pathway analysis were performed employing Metascape software, where inputs were identified from our systematic review of differentially expressed genes in overactive bladder. A total of 9 studies were included in the final analysis and 11 genes were identified as being up-regulated (purinergic receptor P2X 2 [P2RX2], smoothelin [SMTN], growth-associated protein 43 [GAP43], transient receptor potential cation channel subfamily M member 8 [TRPM8], cadherin 11 [CDH1], gap junction protein gamma 1 [GJC1], cholinergic receptor muscarinic 2 [CHRM2], cholinergic receptor muscarinic 3 [CHRM3], and transient receptor potential cation channel subfamily V member 4 [TRPV4]) or down-regulated (purinergic receptor P2X 2 [P2RX3] and purinergic receptor P2X 5 [P2RX5]) in patients with overactive bladder. Gene network analysis showed that genes are involved in chemical synaptic transmission, smooth muscle contraction, blood circulation, and response to temperature stimulus. Network analysis demonstrated a significant genetic interaction between TRPV4, TRPM8, P2RX3, and PR2X2 genes. Outcomes of this systematic review highlighted potential biomarkers for treatment efficacy and have laid the groundwork for developing future gene therapies for overactive bladder in clinical settings." @default.
- W4289755521 created "2022-08-04" @default.
- W4289755521 creator A5000769878 @default.
- W4289755521 creator A5002253189 @default.
- W4289755521 creator A5002362509 @default.
- W4289755521 creator A5005644749 @default.
- W4289755521 creator A5008073132 @default.
- W4289755521 creator A5017917826 @default.
- W4289755521 creator A5041987495 @default.
- W4289755521 creator A5044873550 @default.
- W4289755521 creator A5053597509 @default.
- W4289755521 creator A5054621956 @default.
- W4289755521 creator A5056925121 @default.
- W4289755521 creator A5059393407 @default.
- W4289755521 date "2023-01-01" @default.
- W4289755521 modified "2023-09-30" @default.
- W4289755521 title "A systematic review and in silico study of potential genetic markers implicated in cases of overactive bladder" @default.
- W4289755521 cites W1267586634 @default.
- W4289755521 cites W1498579390 @default.
- W4289755521 cites W1623121663 @default.
- W4289755521 cites W1989637542 @default.
- W4289755521 cites W1997752151 @default.
- W4289755521 cites W2003228611 @default.
- W4289755521 cites W2003587769 @default.
- W4289755521 cites W2005225272 @default.
- W4289755521 cites W2010651323 @default.
- W4289755521 cites W2014267662 @default.
- W4289755521 cites W2019182826 @default.
- W4289755521 cites W2021184142 @default.
- W4289755521 cites W2033950000 @default.
- W4289755521 cites W2044332414 @default.
- W4289755521 cites W2055604814 @default.
- W4289755521 cites W2069052757 @default.
- W4289755521 cites W2097795961 @default.
- W4289755521 cites W2111752334 @default.
- W4289755521 cites W2120475330 @default.
- W4289755521 cites W2124649441 @default.
- W4289755521 cites W2126229620 @default.
- W4289755521 cites W2134182567 @default.
- W4289755521 cites W2136114035 @default.
- W4289755521 cites W2150371994 @default.
- W4289755521 cites W2156098321 @default.
- W4289755521 cites W2156346381 @default.
- W4289755521 cites W2160035320 @default.
- W4289755521 cites W2162569984 @default.
- W4289755521 cites W2162880098 @default.
- W4289755521 cites W2166025830 @default.
- W4289755521 cites W2171967342 @default.
- W4289755521 cites W2289015321 @default.
- W4289755521 cites W2327851328 @default.
- W4289755521 cites W2395959860 @default.
- W4289755521 cites W2460574431 @default.
- W4289755521 cites W2471276740 @default.
- W4289755521 cites W2497404211 @default.
- W4289755521 cites W2560438049 @default.
- W4289755521 cites W2593185740 @default.
- W4289755521 cites W2612669776 @default.
- W4289755521 cites W2749020828 @default.
- W4289755521 cites W2790669334 @default.
- W4289755521 cites W2805557898 @default.
- W4289755521 cites W2911684772 @default.
- W4289755521 cites W2928665623 @default.
- W4289755521 cites W2959416930 @default.
- W4289755521 cites W2974663997 @default.
- W4289755521 cites W2978320165 @default.
- W4289755521 cites W2989104765 @default.
- W4289755521 cites W2990063756 @default.
- W4289755521 cites W2991792334 @default.
- W4289755521 cites W2993843753 @default.
- W4289755521 cites W3000079205 @default.
- W4289755521 cites W3043287600 @default.
- W4289755521 cites W3046035961 @default.
- W4289755521 cites W3082702356 @default.
- W4289755521 cites W3087069791 @default.
- W4289755521 cites W3102679918 @default.
- W4289755521 cites W3135696837 @default.
- W4289755521 cites W3166009189 @default.
- W4289755521 cites W3168116216 @default.
- W4289755521 cites W3179782900 @default.
- W4289755521 cites W3193034465 @default.
- W4289755521 cites W4249883463 @default.
- W4289755521 doi "https://doi.org/10.1016/j.ajog.2022.07.044" @default.
- W4289755521 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35932882" @default.
- W4289755521 hasPublicationYear "2023" @default.
- W4289755521 type Work @default.
- W4289755521 citedByCount "2" @default.
- W4289755521 countsByYear W42897555212023 @default.
- W4289755521 crossrefType "journal-article" @default.
- W4289755521 hasAuthorship W4289755521A5000769878 @default.
- W4289755521 hasAuthorship W4289755521A5002253189 @default.
- W4289755521 hasAuthorship W4289755521A5002362509 @default.
- W4289755521 hasAuthorship W4289755521A5005644749 @default.
- W4289755521 hasAuthorship W4289755521A5008073132 @default.
- W4289755521 hasAuthorship W4289755521A5017917826 @default.
- W4289755521 hasAuthorship W4289755521A5041987495 @default.
- W4289755521 hasAuthorship W4289755521A5044873550 @default.
- W4289755521 hasAuthorship W4289755521A5053597509 @default.
- W4289755521 hasAuthorship W4289755521A5054621956 @default.