Evidence map›Paper›PMID 41975084›Full record

ArticleEMBO molecular medicine2026

Microvascular endothelial scavenger receptor class B type I protects against heart failure with preserved ejection fraction by inhibiting T-cell cardiotropism.

Yufei Wu, Xiaomei Yang, Yu Bai, Chenze Li, Peng Wang, Qing Xu, Hui Li, Xiaoli Rao, Yangkai Xu, Jie Chen and 16 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EMBO molecular medicine, 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
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

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

26 authors.

Yufei Wu *The Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China.
Xiaomei Yang *Department of Anesthesiology, Qilu Hospital of Shandong University, Jinan, China.
Yu BaiState Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, China.
Chenze LiDepartment of Cardiology, Zhongnan Hospital of Wuhan University, Institute of Myocardial Injury and Repair, Wuhan University, Wuhan, China.
Peng WangCardiac Department, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China.
Qing XuCore Facilities Centre, Capital Medical University, Beijing, China.
Hui LiDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.ORCID 0000-0002-2108-0201
Xiaoli RaoDepartment of Medical Genetics, Center for Medical Genetics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yangkai XuThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China.
Jie ChenThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China.
Huanhuan CaoThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China.
Qi ZhangThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China.
Mingming ZhaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.
Rui ZhanResearch Center for Cardiopulmonary Rehabilitation, University of Health and Rehabilitation Sciences Qingdao Hospital (Qingdao Municipal Hospital), School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao, China.
Xue FanClinical Research Institute, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuedong HouDepartment of Anesthesiology, Qilu Hospital of Shandong University, Jinan, China.
Jie LiuState Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai Heart Failure Research Center, Department of Cardiovascular Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Hong S LuDepartment of Physiology, Saha Cardiovascular Research Center and Saha Aortic Center, University of Kentucky, Lexington, KY, USA.ORCID 0000-0002-0577-2558
Tianyun WangDepartment of Medical Genetics, Center for Medical Genetics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.ORCID 0000-0002-5179-087X
Wei Dong GaoDepartment of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Linzhang HuangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Fudan University, Shanghai, China.ORCID 0000-0002-9092-2855
Han XiaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.ORCID 0000-0003-4124-9411
Lingyun ZuDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.
Alan DaughertyDepartment of Physiology, Saha Cardiovascular Research Center and Saha Aortic Center, University of Kentucky, Lexington, KY, USA.ORCID 0000-0003-2093-3775
Mingguo XuDepartment of Pediatrics, The Third People's Hospital of Longgang, Clinical Institute of Shantou University Medical College, Shenzhen, China. docjxzhu@stu.edu.cn.ORCID 0000-0002-8215-7065
Lemin ZhengThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing, China. zhengl@bjmu.edu.cn.ORCID 0000-0003-4473-6936

Funding

fundamental research funds for the central universities, peking university medicine sailing program for young scholars's scientific & technological innovation BMU2023YFJHPY027Fundamental research funds for the central universities starting fund BMU2022RCZX038Guangdong Pharmaceutical University Shenzhen Hospital (Longgang) and Guangdong Pharmaceutical University LGSY 202302National Key Research and Development Program of China (NKPs) 2023YFA1800904National Key Research and Development Program of China (NKPs) 2025ZD0549600national natural science foundation of china 82201314national nature science foundation of china 81870364Shandong provincial natural science foundation ZR2022MH052Special Fund for Medical and Health Technology Innovation Projects, Longgang District Science andTechnology Innovation Program, Shenzhen LGKCYLWS2022035Special Fund for Medical and Health Technology Innovation Projects, Longgang District Science andTechnology Innovation Program, Shenzhen LGKCYLWS2025-34Special Fund for Medical and Health Technology Innovation Projects, Longgang District Science andTechnology Innovation Program, Shenzhen LGWJ2024-93the china postdoctoral science foundation NO.2021M691944the national natural science foundation of china U25A2011the National Natural Science Foundation of China U22A20286the natural science foundation of beijing, china 7242163the natural Science foundation of beijing, china L232031the Natural Science Foundation of Beijing, China J230039
6 · The paper itself

Abstract

Cardiac microvascular endothelial cells (CMECs) dysfunction is a well-recognized mediator of heart failure with preserved ejection fraction (HFpEF), but the underlying mechanism remains unclear. Here we find that scavenger receptor class B type I (SR-B1) is predominantly expressed in CMECs and decreased significantly in HFpEF. Endothelial-specific SR-B1 deficiency exacerbates cardiac pathological remodeling and diastolic dysfunction in HFpEF, which can be prevented by endothelial SR-B1 reconstitution through adeno-associated virus serotype 1 (AAV1)-mediated delivery in endothelial-specific SR-B1-deficient mice. Single-cardiac-endothelial-cell transcriptomics and lineage-tracing system reveal that inflammatory CMECs subcluster activation is responsible for the deteriorating HFpEF progression induced by endothelial SR-B1 loss, rather than endothelial-to-mesenchymal transition. Mechanistically, SR-B1 loss drives increased CXCL10 secretion, which orchestrates CMECs activation and CXCR3-positive T-cell cardiotropism to promote diastolic dysfunction-a process associated with endothelial IRF1 activation. Most importantly, the SR-B1-CXCL10-CXCR3 axis is activated in human HFpEF cardiac tissue, and the elevated CXCL10 level in plasma is independently associated with a higher HFpEF prevalence. This study uncovers that activation of the SR-B1-CXCL10-CXCR3 axis in CMECs aggravates HFpEF pathogenesis through the accumulation of CXCR3-positive T-cells in hearts.

Indexed as

Endothelial CellsHeart FailureScavenger Receptors, Class BT-LymphocytesAnimalsHumansMaleMiceMice, Inbred C57BLMice, KnockoutStroke VolumeScavenger Receptors, Class BCardiac Microvascular Endothelial DysfunctionChemokine C-X-C Motif Chemokine Ligand 10 (CXCL10)Heart Failure with Preserved Ejection FractionScavenger Receptor Class B Type I (SR-B1)

Identifiers

PMID41975084
PMCPMC13179366

What Socratic holds

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LicenceCC BY
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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 Socratic graph.