Evidence map›Paper›PMID 32547719›Full record

ArticleTherapeutic advances in chronic disease2020

Alisol B 23-acetate attenuates CKD progression by regulating the renin-angiotensin system and gut-kidney axis.

Hua Chen, Min-Chang Wang, Yuan-Yuan Chen, Lin Chen, Yan-Ni Wang, Nosratola D Vaziri, Hua Miao, Ying-Yong Zhao

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in chronic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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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

8 authors at 2 institutions in 2 countries.

Hua ChenFaculty of Life Science & Medicine, Northwest University, Xi'an, Shaanxi, China.
Min-Chang WangInstrumental Analysis Center, Xi'an Modern Chemistry Institute, Xi'an, Shaanxi, China.
Yuan-Yuan ChenFaculty of Life Science & Medicine, Northwest University, Xi'an, Shaanxi, China.
Lin ChenFaculty of Life Science & Medicine, Northwest University, Xi'an, Shaanxi, China.
Yan-Ni WangFaculty of Life Science & Medicine, Northwest University, Xi'an, Shaanxi, China.
Nosratola D VaziriDivision of Nephrology and Hypertension, School of Medicine, University of California Irvine, CA, USA.
Hua MiaoFaculty of Life Science & Medicine, Northwest University, Xi'an, Shaanxi, China.
Ying-Yong ZhaoFaculty of Life Science & Medicine, Northwest University, No. 229 Taibai North Road, Xi'an, Shaanxi 710069, China.ORCID https://orcid.org/0000-0002-0239-7342
Northwest University · CNUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidence suggests a link between the gut microbiome and various diseases including hypertension and chronic kidney disease (CKD). However, studies examining the efficacy of controlling blood pressure and inhibiting the renin-angiotensin system (RAS) in preventing CKD progression are limited.

methodsIn the present study, we used 5/6 nephrectomised (NX) and unilateral ureteral obstructed (UUO) rat models and cultured renal tubular epithelial cells and fibroblasts to test whether alisol B 23-acetate (ABA) can attenuate renal fibrogenesis by regulating blood pressure and inhibiting RAS.

resultsABA treatment re-established dysbiosis of the gut microbiome, lowered blood pressure, reduced serum creatinine and proteinuria, suppressed expression of RAS constituents and inhibited the epithelial-to-mesenchymal transition in NX rats. Similarly, ABA treatment inhibited expression of collagen I, fibronectin, vimentin, α-smooth muscle actin and fibroblast-specific protein 1 at both mRNA and protein levels in UUO rats. ABA was also effective in suppressing activation of the transforming growth factor-β (TGF-β)/Smad3 and preserving Smad7 expression in both NX and UUO rats.

conclusionThese data suggest that ABA attenuated renal fibrosis through a mechanism associated with re-establishing dysbiosis of the gut microbiome and regulating blood pressure, and Smad7-mediated inhibition of Smad3 phosphorylation. Thus, we demonstrate ABA as a promising candidate for treatment of CKD by improving the gut microbiome and regulating blood pressure.

Indexed as

alisol B 23-acetatechronic kidney diseasegut microbiomehypertensionrenal fibrosisrenin–angiotensin system

Identifiers

PMID32547719
PMCPMC7249553
OpenAlexW3026462996

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.