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
9 authors.
Di ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0009-0003-4927-8265 Jiayu LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0000-0001-5086-5502 Yueqi LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0000-0001-5194-8238 Zhenhui LiangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.
Ke GuiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0009-0005-6489-2890 Weijuan YaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0000-0003-4698-612X Xiaohong WangDepartment of Pharmacology, Tianjin Key Laboratory of Inflammation Biology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Sciences, Laboratory of Molecular Ophthalmology and Tianjin Key Laboratory of Ocular Trauma, Tianjin Medical University, Tianjin 300070, China.ORCID 0000-0001-8628-243X Jing ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing 100191, China.ORCID 0000-0002-2211-4901 Funding
No grant is acknowledged in the PubMed record.
6 · The paper itselfAbstract
Endothelial cell (EC) mechanosensing is essential for vascular homeostasis and atherosclerosis development, though the influence of blood flow patterns on EC signaling is not fully understood. Discoidin domain receptor 1 (DDR1), a tyrosine kinase receptor, acts as a mechanosensor linking shear force to endothelial responses. Atheroprotective laminar shear flow induces rapid, transient DDR1 activation and condensation through liquid-liquid phase separation without harmful effects, while atherogenic shear causes delayed, sustained condensation, leading to Yes-associated protein (YAP) activation and downstream pathological signaling. We show that heat shock protein 27 (HSP27) regulates shear-dependent DDR1 condensation and phase transition. Specifically, the interaction between DDR1 and HSP27, mediated by their respective domains, is crucial for DDR1 condensate disassembly. Atherogenic shear, unlike atheroprotective shear, triggers prolonged DDR1-mediated HSP27 phosphorylation, promoting DDR1 gel transition and activating YAP signaling. The DDR1-HSP27 axis is key in endothelial YAP activation and atherogenesis in vivo. Targeting this pathway may offer therapeutic potential for preventing endothelial dysfunction and atherosclerosis.
Indexed as
Discoidin Domain Receptor 1HSP27 Heat-Shock ProteinsMolecular ChaperonesPhase TransitionAdaptor Proteins, Signal TransducingAnimalsAtherosclerosisEndothelial CellsHeat-Shock ProteinsHumansMechanotransduction, CellularPhase SeparationPhosphorylationSignal TransductionYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingDDR1 protein, humanDiscoidin Domain Receptor 1Heat-Shock ProteinsHSP27 Heat-Shock ProteinsHSPB1 protein, humanMolecular ChaperonesYAP-Signaling Proteins
Identifiers
PMID42599996
PMCPMC13475575
What OpenQuestion holds
Textmetadata
Read underepoch 390