ArticleLife sciences2018
Urinary bladder organ hypertrophy is partially regulated by Akt1-mediated protein synthesis pathway.
Article in Life sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- TRPC3 contributes to cyclophosphamide-induced cystitis progression by enhancing bladder fibrosis through activation of the TGF-β/smad pathway.Frontiers in pharmacology · 2025Article
- Effect of moderate-intensity aerobic exercise on bladderNarra J · 2024Article
- Fibrotic Diseases of the Human Urinary and Genital Tract: Current Understanding and Potential Strategies for Treatment.Journal of clinical medicine · 2023Review
- YAP-mediated mechanotransduction in urinary bladder remodeling: Based on RNA-seq and CUT&Tag.Frontiers in genetics · 2023Article
- Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder.Scientific reports · 2021Article
- Microbiota Alters Urinary Bladder Weight and Gene Expression.Microorganisms · 2020Article
- Recommendations for evaluation of bladder and bowel function in pre-clinical spinal cord injury research.The journal of spinal cord medicine · 2020Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
aimsThe present study aims to investigate the role of Akt in the regulation of urinary bladder organ hypertrophy caused by partial bladder outlet obstruction (pBOO). MAIN
methodsMale rats were surgically induced for pBOO. Real-time PCR and western blot were used to examine the levels of mRNA and protein. A phosphoinositide 3-kinase (PI3K) inhibitor LY294002 was used to inhibit the activity of endogenous Akt. KEY
findingsThe urinary bladder developed hypertrophy at 2 weeks of pBOO. The protein but not mRNA levels of type I collagen and α-smooth muscle actin (αSMA) were increased in pBOO bladder when compared to sham control. The phosphorylation (activation) levels of Akt1 (p-Ser SIGNIFICANCE: pBOO-induced urinary bladder hypertrophy is attributable to fibrosis, smooth muscle cellular hypertrophy, and urothelium cell hyper-proliferation. Akt1-mediated protein synthesis in pBOO bladder contributes to type I collagen and αSMA but not PCNA up-regulation. Target of Akt1 is necessary but not sufficient in treatment of urinary bladder hypertrophy following pBOO.
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Registered trials
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