Evidence map›Paper›PMID 40391441›Full record

ArticleCirculation research2025

Spleen-Heart Cross-Talk Through CD23-Mediated Signal Promotes Cardiac Remodeling.

Yufan Feng, Yang Yang, Hongqin Yang, Jin Shan, Jiaxin Zhang, Qian Chen, Yingge Zhang, Yarong Zhang, Zhiwei Li, Yunfei Xue and 5 more

Abstract read
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In one paragraph

Article in Circulation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Yufan Feng *Department of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0009-0009-5980-965X
Yang Yang *Department of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Hongqin Yang *Department of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0009-0008-8764-172X
Jin ShanDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Jiaxin ZhangDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Qian ChenDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Yingge ZhangDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Yarong ZhangDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Zhiwei LiDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0000-0001-8031-6547
Yunfei XueDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).
Junye ChenDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0000-0001-9224-1677
Chi GengDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0000-0002-9737-7271
Kegang JiaDepartment of Clinical Laboratory, TEDA International Cardiovascular Hospital, Tianjin, China (K.J.).
Hongmei ZhaoDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0009-0007-3908-3316
Jing WangDepartment of Pathophysiology, Chinese Academy of Medical Sciences, School of Basic Medicine, Institute of Basic Medicine, Peking Union Medical College, Beijing (Y.F., Y.Y., H.Y., J.S., J.Z., Q.C., Yingge Zhang, Yarong Zhang, Z.L., Y.X., J.C., C.G., H.Z., J.W.).ORCID 0000-0003-2410-5408

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundElevated levels of IgE are implicated in pathological cardiac remodeling. However, the origin of IgE remains unknown. In the current study, we aim to explore the source of IgE and the mechanisms underlying IgE production in the context of pathological cardiac remodeling.

methodsFlow cytometry was used to assess the changes of IgE-producing B cells in different organs/tissues, including the spleen, lymph nodes, bone marrow, peripheral blood, vasculature, and heart, in mice with cardiac remodeling induced by transverse aortic constriction (TAC). The role of IgE low-affinity receptor FcεRII (Fc epsilon receptor II, also named CD23) in IgE-producing B cells during cardiac remodeling was evaluated in mice with loss-of-CD23 or gain-of-CD23. The therapeutic potential of the CD23-neutralizing antibody was evaluated. The factors involved in organ cross-talk, which regulate IgE production, were identified and validated both in vitro and in vivo.

resultsWe found that splenic IgE-producing cells were significantly elevated in the TAC mice. CD23, as a negative regulator of IgE production, was decreased in splenic B cells of TAC mice. Global knockout of CD23 in mice aggravated TAC-induced IgE synthesis and cardiac remodeling in vivo. In contrast, global or B-cell-specific CD23 overexpression in mice reduced IgE synthesis and alleviated TAC-induced cardiac remodeling. Mechanistically, CD23 was cleaved by ADAM10 (A disintegrin and metalloproteinase domain 10) in the spleen. Screening assay with data-independent acquisition mass spectrometry-based proteomics and ELISA identified Ltf (lactotransferrin), released from the heart shortly after TAC stimulation, as a contributor to ADAM10 upregulation through binding to Ltf receptor Ncl (nucleolin). Meanwhile, Ltf administration promoted IgE elevation, accompanied by increased ADAM10 expression and decreased CD23 expression in vitro and in vivo. Furthermore, the plasma Ltf levels were positively correlated with TAC-induced cardiac remodeling, serum IgE, and sCD23 (soluble CD23). Consistently, Ltf levels were elevated in patients with heart failure with reduced ejection fraction and also positively correlated with serum IgE and sCD23.

conclusionsOur findings indicate a critical role of the Ltf-ADAM10-CD23 axis in regulating IgE production through cross-talk between the heart and spleen. The Ltf-ADAM10-CD23 axis may represent new molecular targets for IgE-mediated pathological cardiac remodeling.

Indexed as

Receptors, IgESpleenVentricular RemodelingADAM10 ProteinAmyloid Precursor Protein SecretasesAnimalsB-LymphocytesImmunoglobulin EMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutSignal TransductionADAM10 ProteinAdam10 protein, mouseAmyloid Precursor Protein SecretasesImmunoglobulin EMembrane ProteinsReceptors, IgEheart failureimmunoglobulin Espleen

Identifiers

PMID40391441

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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.