Evidence map›Paper›PMID 31164038›Full record

ArticleCell cycle (Georgetown, Tex.)2019

Methionine restriction delays senescence and suppresses the senescence-associated secretory phenotype in the kidney through endogenous hydrogen sulfide.

Si-Yang Wang, Wen-Juan Wang, Jie-Qiong Liu, Yu-Huan Song, Ping Li, Xue-Feng Sun, Guang-Yan Cai, Xiang-Mei Chen

Abstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

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  18. mTOR Complex 1 Content and Regulation Is Adapted to Animal Longevity.International journal of molecular sciences · 2022
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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.

Si-Yang Wanga Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Wen-Juan Wanga Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Jie-Qiong Liua Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Yu-Huan Songa Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Ping Lia Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Xue-Feng Suna Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Guang-Yan Caia Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.
Xiang-Mei Chena Department of Nephrology, Chinese PLA General Hospital , Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases , Beijing , China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a risk factor for various acute and chronic kidney injuries. Kidney aging is accompanied by the secretion of growth factors, proteases, and inflammatory cytokines, known as the senescence-associated secretory phenotype (SASP). These factors accelerate the aging process and senescence-associated changes. Delaying kidney senescence may prevent acute and chronic kidney injury. Methionine restriction (MR) was found to be an effective intervention for delaying senescence. However, the mechanism of MR remains unclear. In this study, we investigated the effect of MR on the survival rate and renal aging of C57BL/6 mice and examined the relevant mechanisms. MR increased the survival rate and decreased the levels of senescence markers in the aging kidney. Both in vivo and in vitro, MR upregulated the transsulfuration pathway to increase H

Indexed as

AgingAMP-Activated Protein KinasesAnimalsCaloric RestrictionCell LineCellular SenescenceCystathionine gamma-LyaseCytokinesHumansHydrogen SulfideIndicanKidneyKidney DiseasesLongevityMaleMethionineAMP-Activated Protein KinasesCystathionine gamma-LyaseCytokinesHydrogen SulfideIndicanMethionineTOR Serine-Threonine Kinaseshydrogen sulfidemethionine restrictionrenalSenescencesenescence-associated secretory phenotype

Identifiers

PMID31164038
PMCPMC6619995

What OpenQuestion holds

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Registered trials

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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.