In one paragraphArticle in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
16 authors.
Wu-Wei RongDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-0257-1678 Zi-Qi XuDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0008-1770-4203 Shuai ShaoDepartment of Vascular & Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0008-4248-6025 Qian-Wan DengDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0002-9309-8352 Meng-Yao LiDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0003-0315-2464 Jin-Qiu WeiDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0002-8924-3625 Yi-Hang YangDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0006-1461-3002 Jia-Jia ZhaoDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0004-7747-2484 Wen-Hui ZhaiDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0008-6771-9286 Zhi-Wen ShangDepartment of Vascular & Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0001-7411-4751 Zhi ZhangDepartment of Vascular & Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-0253-8192 Wen-Yi YangDepartment of Vascular & Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-1279-0866 Shao-Wen LiuDepartment of Vascular & Cardiology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ping-Jin GaoDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-7750-3314 Xiao-Dong LiDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-3771-6286 Ji-Guang WangDepartment of Cardiovascular Medicine, National Research Center for Translational Medicine·Shanghai, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
Macrophages play a key role in cardiac injury and repair after myocardial infarction (MI). Salt-inducible kinase 2 (SIK2), a member of the adenosine monophosphate-activated protein kinase family, is notably up-regulated in monocytes/macrophages of patients with MI and animal models. In this study, we investigated the role of SIK2 in macrophage-mediated inflammation and efferocytosis following MI. Macrophage-specific SIK2 deletion reduces infarct size and improves healing post-MI. Furthermore, SIK2-knockout macrophages decrease proinflammatory factor expression and enhance efferocytosis, thereby increasing repair factors expression. SIK2 associates with tumor necrosis factor receptor-associated factor 2 (TRAF2), promoting its phosphorylation and K63 polyubiquitylation, which exacerbates inflammation and hinders efferocytosis via the P38 and nuclear factor κB pathways. In contrast, the SIK2
Indexed as
MacrophagesMyocardial InfarctionProtein Serine-Threonine KinasesAnimalsDisease Models, AnimalEfferocytosisHumansInflammationMaleMiceMice, KnockoutNF-kappa Bp38 Mitogen-Activated Protein KinasesTNF Receptor-Associated Factor 2UbiquitinationNF-kappa Bp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesTNF Receptor-Associated Factor 2TRAF2 protein, mouse
Identifiers
PMID42886791
PMCPMC13674512
What OpenQuestion holds
Textmetadata
Read underepoch 390