Evidence map›Paper›PMID 42657466›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2026

Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.

Bruno De Souza Goncalves, Yaxin Wang, Sneha S Pillai, Quoc Quang Luu, Hortense Triniac, Hari Vishal Lakhani, Muhammad A Chaudhry, Ze Zheng, Joseph I Shapiro, Roy L Silverstein and 2 more

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Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Bruno De Souza Goncalves *Department of Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV (B.D.S.G., S.S.P., H.V.L., M.A.C., K.S.).ORCID 0009-0003-8733-2613
Yaxin Wang *Versiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0003-0695-3542
Sneha S PillaiDepartment of Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV (B.D.S.G., S.S.P., H.V.L., M.A.C., K.S.).
Quoc Quang LuuVersiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0003-2183-8171
Hortense TriniacVersiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0003-1835-7959
Hari Vishal LakhaniDepartment of Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV (B.D.S.G., S.S.P., H.V.L., M.A.C., K.S.).ORCID 0000-0002-5308-2164
Muhammad A ChaudhryDepartment of Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV (B.D.S.G., S.S.P., H.V.L., M.A.C., K.S.).
Ze ZhengVersiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0002-4453-224X
Joseph I ShapiroDepartment of Medicine, University of Toledo, OH (J.I.S.).
Roy L SilversteinVersiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0001-7859-9154
Komal SodhiDepartment of Surgery, and Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV (B.D.S.G., S.S.P., H.V.L., M.A.C., K.S.).ORCID 0000-0002-1179-2985
Yiliang ChenVersiti Blood Research Institute, Milwaukee, WI (Y.W., Q.Q.L., H.T., Z.Z., R.L.S., Y.C.).ORCID 0000-0001-9786-8305

Funding

NKA/CD36 signaling in adipocytes promotes oxidative stress and drives chronic inflammation in atherosclerosisR01HL164460 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI Yiliang Chen, Roy L Silverstein · 2023 to 2026
$2.1M
NHLBI NIH HHS R01 HL164460
6 · The paper itself

Abstract

backgroundAdipocyte dysfunction is closely associated with oxidative stress and chronic inflammation, which contribute to systemic metabolic disturbances and atherosclerosis. We previously identified the NKA (Na/K-ATPase) α1 subunit as a signal transducer that activates Src-family kinases and promotes oxidative stress and inflammation in various cell types, including adipocytes and macrophages. NaKtide, a peptide inhibitor of NKA signaling, has been shown to reduce systemic oxidative stress and inflammation in vivo. In this study, we investigated the role of adipocyte-specific NKA signaling in atherosclerosis.

methodsAdipocyte-specific NaKtide was delivered to

resultsAdipocyte-specific NaKtide reduced atherosclerotic plaque area by 67% in the aortic arch and by 48% in the aortic sinus. CD68+ (cluster of differentiation 68) macrophage content and α-SMA+ (α-smooth muscle actin) smooth muscle cell content in the aortic sinus were decreased by 45% and 53%, respectively. These vascular improvements were accompanied by dampened adipose tissue inflammation and oxidative stress, improved glucose tolerance, and reduced systemic inflammation.

conclusionsThese findings highlight a critical contributing role for adipocyte NKA signaling in atherosclerosis, suggesting an important endocrine and paracrine influence of adipose tissue on large artery atherogenesis and supporting the therapeutic potential of targeting NKA in cardiometabolic disease.

Indexed as

AdipocytesAorta, ThoracicAortic DiseasesAtherosclerosisSignal TransductionSodium-Potassium-Exchanging ATPaseAnimalsDiet, WesternDisease Models, AnimalInflammation MediatorsMacrophagesMaleMiceMice, Inbred C57BLMice, Knockout, ApoEOxidative StressInflammation MediatorsSodium-Potassium-Exchanging ATPasesrc-Family Kinasesadipocytesatherosclerosisinflammationoxidative stresssrc-family kinases

Identifiers

PMID42657466
PMCPMC13523103

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.