Evidence map›Paper›PMID 38375634›Full record

ArticleCirculation research2024

Gsα Regulates Macrophage Foam Cell Formation During Atherosclerosis.

Chang Ma, Yihui Li, Mi Tian, Qiming Deng, Xiaoteng Qin, Hanlin Lu, Jiangang Gao, Min Chen, Lee S Weinstein, Mei Zhang and 5 more

Open access · greenAbstract read
In one paragraph

Article in Circulation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
8.4field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 35 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

15 authors at 4 institutions in 3 countries.

Chang MaNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0001-6285-5598
Yihui LiNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0001-8795-8286
Mi TianDepartment of Cardiology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Shandong Medicine and Health Key Laboratory of Cardiac Electrophysiology and Arrhythmia, Jinan, China (M.T.).
Qiming DengNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).
Xiaoteng QinNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).
Hanlin LuNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0003-1015-2924
Jiangang GaoSchool of Life Science and Key Laboratory of the Ministry of Education for Experimental Teratology (J.G.), Shandong University, Jinan, China.
Min ChenMetabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD (M.C., L.S.W.).
Lee S WeinsteinMetabolic Diseases Branch, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD (M.C., L.S.W.).ORCID 0000-0002-1899-5152
Mei ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0001-6295-5070
Peili BuNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).
Jianmin YangNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0002-8593-2338
Yun ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0003-4432-6144
Cheng ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0003-3672-6543
Wencheng ZhangNational Key Laboratory for Innovation and Transformation of Luobing Theory; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences; Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China (C.M., Y.L., Q.D., X.Q., H.L., M.Z., P.B., J.Y., Y.Z., C.Z., W.Z.).ORCID 0000-0002-9416-6540
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNational Institute of Diabetes and Digestive and Kidney Diseases · USShandong Provincial QianFoShan Hospital · CNShandong University · CN

Funding

Role of the Gnas Gene in Metabolic RegulationZIADK043313 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI WEINSTEIN, LEE · 2009 to 2025
$4.9M
Intramural NIH HHS ZIA DK043313
6 · The paper itself

Abstract

backgroundMany cardiovascular pathologies are induced by signaling through G-protein-coupled receptors via Gsα (G protein stimulatory α subunit) proteins. However, the specific cellular mechanisms that are driven by Gsα and contribute to the development of atherosclerosis remain unclear.

methodsHigh-throughput screening involving data from single-cell and bulk sequencing were used to explore the expression of Gsα in atherosclerosis. The differentially expression and activity of Gsα were analyzed by immunofluorescence and cAMP measurements. Macrophage-specific Gsα knockout (Mac-Gsα

resultsScRNA-seq showed elevated

conclusionsGsα activation is enhanced during atherosclerotic progression and increases lipid uptake and foam cell formation. The genetic or chemical inactivation of Gsα inhibit the development of atherosclerosis in mice, suggesting that drugs targeting Gsα may be useful in the treatment of atherosclerosis.

Indexed as

AtherosclerosisPlaque, AtheroscleroticAnimalsChromograninsFoam CellsGTP-Binding Protein alpha Subunits, GsHumansLipoproteins, LDLMacrophagesMiceSignal TransductionChromograninsGNAS protein, humanGnas protein, mouseGTP-Binding Protein alpha Subunits, GsLipoproteins, LDLatherosclerosischolesterolfoam cellmacrophage

Identifiers

PMID38375634
PMCPMC10978275
OpenAlexW4391985656

What OpenQuestion holds

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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.