Evidence map›Paper›PMID 37291105›Full record

ReviewSignal transduction and targeted therapy2023

Inflammation and aging: signaling pathways and intervention therapies.

Xia Li, Chentao Li, Wanying Zhang, Yanan Wang, Pengxu Qian, He Huang

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 885 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
885citing papers in PubMed, 1 pooled it
200.5field-weighted citation impact, top 1% 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

885 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,143 citations in OpenAlex.

  1. Pooled it
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  14. Functional Shift of NLRP3 Inflammasome Activity in Aged Macrophages.Bulletin of experimental biology and medicine · 2026
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825 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Xia Li *Bone Marrow Transplantation Center, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China.
Chentao Li *Liangzhu Laboratory, Zhejiang University Medical Center, 1369 West Wenyi Road, Hangzhou, 311121, China.
Wanying Zhang *Zhejiang University-University of Edinburgh Institute, Zhejiang University School of Medicine, Zhejiang University, Haining, China.
Yanan Wang *Zhejiang University-University of Edinburgh Institute, Zhejiang University School of Medicine, Zhejiang University, Haining, China.ORCID 0000-0003-4947-8665
Pengxu QianLiangzhu Laboratory, Zhejiang University Medical Center, 1369 West Wenyi Road, Hangzhou, 311121, China. axu@zju.edu.cn.ORCID 0000-0001-5636-6704
He HuangBone Marrow Transplantation Center, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, People's Republic of China. huanghe@zju.edu.cn.ORCID 0000-0002-2723-1621
Zhejiang University-University of Edinburgh Institute · CNZhejiang Lab · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81900176National Natural Science Foundation of China (National Science Foundation of China) 82161138028National Natural Science Foundation of China (National Science Foundation of China) 82222003National Natural Science Foundation of China (National Science Foundation of China) 92268117
6 · The paper itself

Abstract

Aging is characterized by systemic chronic inflammation, which is accompanied by cellular senescence, immunosenescence, organ dysfunction, and age-related diseases. Given the multidimensional complexity of aging, there is an urgent need for a systematic organization of inflammaging through dimensionality reduction. Factors secreted by senescent cells, known as the senescence-associated secretory phenotype (SASP), promote chronic inflammation and can induce senescence in normal cells. At the same time, chronic inflammation accelerates the senescence of immune cells, resulting in weakened immune function and an inability to clear senescent cells and inflammatory factors, which creates a vicious cycle of inflammation and senescence. Persistently elevated inflammation levels in organs such as the bone marrow, liver, and lungs cannot be eliminated in time, leading to organ damage and aging-related diseases. Therefore, inflammation has been recognized as an endogenous factor in aging, and the elimination of inflammation could be a potential strategy for anti-aging. Here we discuss inflammaging at the molecular, cellular, organ, and disease levels, and review current aging models, the implications of cutting-edge single cell technologies, as well as anti-aging strategies. Since preventing and alleviating aging-related diseases and improving the overall quality of life are the ultimate goals of aging research, our review highlights the critical features and potential mechanisms of inflammation and aging, along with the latest developments and future directions in aging research, providing a theoretical foundation for novel and practical anti-aging strategies.

Indexed as

Cellular SenescenceQuality of LifeHumansInflammationSignal Transduction

Identifiers

PMID37291105
PMCPMC10248351
OpenAlexW4379966446

What OpenQuestion holds

Textmetadata
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.