Evidence map›Paper›PMID 34286232›Full record

ArticleiScience2021

Programmed PPAR-α downregulation induces inflammaging by suppressing fatty acid catabolism in monocytes.

Ming Wang, Yan Yan, Zhengguo Zhang, Xiaohan Yao, Xixi Duan, Ziming Jiang, Junfeng An, Peiguo Zheng, Yijie Han, Hao Wu and 3 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 19 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

13 authors at 5 institutions in 2 countries.

Ming WangMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan 450052, China.
Yan YanMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan 450052, China.
Zhengguo ZhangDepartment of Urology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Xiaohan YaoMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan 450052, China.
Xixi DuanMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan 450052, China.
Ziming JiangDepartment of Urology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Junfeng AnSchool of Yunkang Medical and Health Management, Nanfang College of SUN Yat-Sen University, Guangzhou city, Guangdong 510970, China.
Peiguo ZhengClinical Laboratory, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.
Yijie HanUniversity of Chinese Academy of Sciences, Beijing, China.
Hao WuWürzburg Institute of Systems Immunology, Max-planck Research Group, University Würzburg, Germany.
Zhaoqing WangKey Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
Rainer GlaubenCorporate Member of Freie Universität Berlin, Charité - Universitätsmedizin Berlin, Humboldt-Universität zu Berlin, Berlin, Germany.
Zhihai QinMedical Research Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, Henan 450052, China.
First Affiliated Hospital of Zhengzhou University · CNChinese Academy of Sciences · CNHumboldt-Universität zu Berlin · DESun Yat-sen University · CNUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammaging is associated with an increased risk of chronic disease. Monocytes are the principal immune cells for the production of inflammatory cytokines and contribute to inflammaging in the elderly. However, the underlying mechanisms remain largely unknown. Here, we found that monocytes from aged individuals contained high levels of lipid droplets (LDs), and this increase was correlated with impaired fatty acid oxidation. Downregulated peroxisome proliferator-activated receptor (PPAR)-α may be responsible for the pro-inflammatory phenotype of monocytes in aged individuals, as it was positively correlated with LD accumulation and increasing TNF-α concentration. Interestingly, interventions that result in PPAR-α upregulation, such as fenofibrate treatment, TNF-α neutralization, or calorie restriction, reversed the effect of aging on monocytes. Thus the downregulation of PPAR-α and LD levels in monocytes represents a novel biomarker for inflammaging. Furthermore, PPAR-α activation in the elderly may also alleviate long-term inflammaging, preventing the development of life-limiting chronic diseases.

Indexed as

Cell biologyhuman metabolismImmunology

Identifiers

PMID34286232
PMCPMC8273418
OpenAlexW3175667159

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.