Evidence map›Paper›PMID 30054990›Full record

ArticleJournal of cellular and molecular medicine2018

Acetyl-11-keto-β-boswellic acid ameliorates renal interstitial fibrosis via Klotho/TGF-β/Smad signalling pathway.

Minna Liu, Tianlong Liu, Peijin Shang, Yikai Zhang, Limin Liu, Ting Liu, Shiren Sun

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  6. Article
  7. Article
  8. Review
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  11. Down-regulation of LINC00667 hinders renal tubular epithelial cell apoptosis and fibrosis through miR-34c.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
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  13. Review
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  17. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Minna LiuDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Tianlong LiuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Peijin ShangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Yikai ZhangMedical Equipment Quality Supervision and Inspection Institute, Shaanxi Food and Drug Administration, Xianyang, China.
Limin LiuDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Ting LiuDepartment of Nephrology, the Fourth Hospital of Xi'an, Xi'an, China.
Shiren SunDepartment of Nephrology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0001-5322-1454
Xijing Hospital · CNThe Fourth People's Hospital · CNShandong Institute of Food and Drug Inspection · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl-11-keto-β-boswellic acid (AKBA), an active triterpenoid compound from the extract of Boswellia serrate, has been reported previously in our group to alleviate fibrosis in vascular remodelling. This study aimed to elucidate the in vivo and in vitro efficacy and mechanism of AKBA in renal interstitial fibrosis. The experimental renal fibrosis was produced in C57BL/6 mice via unilateral ureteral obstruction (UUO). Hypoxia-induced HK-2 cells were used to imitate the pathological process of renal fibrosis in vitro. Results showed that the treatment of AKBA significantly alleviated UUO-induced impairment of renal function and improved the renal fibrosis by decreasing the expression of TGF-β1, α-SMA, collagen I and collagen IV in UUO kidneys. In hypoxia-induced HK-2 cells, AKBA displayed remarkable cell protective effects and anti-fibrotic properties by increasing the cell viability, decreasing the lactate dehydrogenase (LDH) release and inhibiting fibrotic factor expression. Moreover, in obstructed kidneys and HK-2 cells, AKBA markedly down-regulated the expression of TGFβ-RI, TGFβ-RII, phosphorylated-Smad2/3 (p-Smad2/3) and Smad4 in a dose-dependent fashion while up-regulated the expression of Klotho and Smad7 in the same manner. In addition, the effects of AKBA on the Klotho/TGF-β/Smad signalling were reversed by transfecting with siRNA-Klotho in HK-2 cells. In conclusion, our findings provide evidence that AKBA can effectively protect kidney against interstitial fibrosis, and this renoprotective effect involves the Klotho/TGF-β/Smad signalling pathway. Therefore, AKBA could be considered as a promising candidate drug for renal interstitial fibrosis.

Indexed as

AnimalsBoswelliaFibrosisGene Expression RegulationGlucuronidaseHumansKidneyKidney DiseasesKlotho ProteinsMiceReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIRNA, Small InterferingSignal TransductionSmad4 ProteinTransforming Growth Factor beta1acetyl-11-ketoboswellic acidGlucuronidaseKlotho ProteinsReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIRNA, Small InterferingSmad4 ProteinSmad4 protein, mouseTgfb1 protein, mouseTgfbr2 protein, mouseTransforming Growth Factor beta1TriterpenesAcetyl-11-keto-β-boswellic acidHK-2 cellsKlotho/TGF-β/Smad signalling pathwayrenal interstitial fibrosisunilateral ureteral obstruction

Identifiers

PMID30054990
PMCPMC6156234
OpenAlexW2884427722

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.