ArticleWorld journal of urology2010
Shock wave induces chronic renal lesion through activation of the nuclear factor kappa B signaling pathway.
Article in World journal of urology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Use of the Shock Wave Therapy in Basic Research and Clinical Applications-From Bench to Bedsite.Biomedicines · 2022Review
- Impact of repeated extracorporeal shock wave lithotripsy on prepubertal rat kidney.Urolithiasis · 2018Article
- Evaluation and physiopathology of minor transient shock wave lithotripsy - induced renal injury based on urinary biomarkers levels.Central European journal of urology · 2018Review
- Autophagy activation protects shock wave induced renal tubular epithelial cell apoptosis may through modulation of Akt/ GSK-3β pathway.International journal of biological sciences · 2016Article
- Shock wave induces biological renal damage by activating excessive inflammatory responses in rat model.Inflammation · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe mechanisms responsible for the pathogenesis of long-term renal damage induced by extracorporeal shock wave lithotripsy (ESWL) are not clear. The present study was designed to investigate the role of nuclear factor κB (NFκB) signal pathway in the pathogenesis of chronic shock wave-induced renal damage in rat model. MATERIALS AND
methodsAdult male Sprague-Dawley rats were exposed to ESWL under the guidance of X-rays. On days 1, 3, 7, 35, and 105 postexposures to shock wave, the animals were killed to examine the changes in renal histology and functions, and NFκB activity. The expression of NFκB-dependent fibrogenic genes was also analyzed. Pyrrolidine dithiocarbamate (PDTC), a specific NFκB inhibitor, was used to further investigate the involvement of NFκB.
resultsThe applied shock wave caused a transient decline in renal function and induced chronic morphological changes such as tubular injury and interstitial fibrosis. NFκB was significantly activated in renal cortex. PDTC had little or no effects on the shock-wave-induced transient renal damage, but attenuated the long-term renal lesions associated with NFκB activation. In addition, the shock wave exposure also up-regulated the expression of transforming growth factor-β1 (TGF-β1), which was also blocked by PDTC.
conclusionNFκB plays an important role in the progression of shock-wave- induced long-term renal damage in rat model.
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Registered trials
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