Evidence map›Paper›PMID 33327751›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2021

SIRT3 (Sirtuin-3) Prevents Ang II (Angiotensin II)-Induced Macrophage Metabolic Switch Improving Perivascular Adipose Tissue Function.

Tong Wei (魏彤), Jing Gao (高晶), Chenglin Huang (黄程淋), Bei Song (宋蓓), Mengwei Sun (孙孟炜), Weili Shen (沈伟利)

Abstract read
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In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

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  15. Roles of SIRT3 in aging and aging-related diseases.International journal of biological sciences · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 3 countries.

Tong Wei (魏彤)Department of Cardiovascular Medicine, Department of Hypertension, and Department of General Practice, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China (T.W., J.G., C.H., B.S., W.S.).
Jing Gao (高晶)Department of Cardiovascular Medicine, Department of Hypertension, and Department of General Practice, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China (T.W., J.G., C.H., B.S., W.S.).
Chenglin Huang (黄程淋)Department of Cardiovascular Medicine, Department of Hypertension, and Department of General Practice, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China (T.W., J.G., C.H., B.S., W.S.).
Bei Song (宋蓓)Department of Cardiovascular Medicine, Department of Hypertension, and Department of General Practice, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China (T.W., J.G., C.H., B.S., W.S.).
Mengwei Sun (孙孟炜)Department of Cardiovascular Medicine, Department of Hypertension, and Department of General Practice, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, China (T.W., J.G., C.H., B.S., W.S.).
Weili Shen (沈伟利)Key Laboratory of State General Administration of Sport, Shanghai Research Institute of Sports Science, China (M.S.).
Shanghai Institute of Hypertension · CNGeneral Administration of Sport of China · CNRuijin Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveInfiltrated macrophages actively promote perivascular adipose tissue remodeling and represent a dominant population in the perivascular adipose tissue microenvironment of hypertensive mice. However, the role of macrophages in initiating metabolic inflammation remains uncertain. SIRT3 (sirtuin-3), a NAD-dependent deacetylase, is sensitive to metabolic status and mediates adaptation responses. In this study, we investigated the role of SIRT3-mediated metabolic shift in regulating NLRP3 (Nod-like receptor family pyrin domain-containing 3) inflammasome activation. Approach and Results: Here, we report that Ang II (angiotensin II) accelerates perivascular adipose tissue inflammation and fibrosis, accompanied by NLRP3 inflammasome activation and IL (interleukin)-1β secretion in myeloid SIRT3 knockout (SIRT3

conclusionsSIRT3 represents a potential therapeutic target to attenuate NLRP3-related inflammation. Pharmacological targeting of glycolytic metabolism may represent an effective therapeutic approach.

Indexed as

Cell PlasticityEnergy MetabolismAcetylationAdipose Tissue, BrownAngiotensin IIAnimalsDisease Models, AnimalFibrosisHEK293 CellsHumansHypertensionInflammasomesInterleukin-1betaLactic AcidMacrophagesMaleAngiotensin IIIL1B protein, mouseInflammasomesInterleukin-1betaLactic AcidNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousepyruvate dehydrogenase E1alpha subunitPyruvate Dehydrogenase (Lipoamide)Sirt3 protein, mouseSirtuin 3angiotensincarnosineinflammasomeinterleukinsirtuin

Identifiers

PMID33327751
OpenAlexW3112418112

What OpenQuestion holds

Textmetadata
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.