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Impact on the Sustainable Development Goals (SDGs)

Analysis of institutional authors

Papaioannou, EleftheriaAuthorCibrian, DanayAuthorSanchez-Madrid, FranciscoAuthorGonzalez-Martin, AliciaAuthorFuster, ValentinAuthor

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July 28, 2025
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Imidazole propionate is a driver and therapeutic target in atherosclerosis

Publicated to: Nature. 645 (8079): 254-261 - 2025-09-04 645(8079), DOI: 10.1038/s41586-025-09263-w

Authors:

Mastrangelo, A; Robles-Vera, I; Mañanes, D; Galán, M; Femenía-Muiña, M; Redondo-Urzainqui, A; Barrero-Rodríguez, R; Papaioannou, E; Amores-Iniesta, J; Devesa, A; Lobo-González, M; Carreras, A; Beck, KR; Ivarsson, S; Gummesson, A; Georgiopoulos, G; Rodrigo-Tapias, M; Martínez-Cano, S; Fernández-López, I; Nuñez, V; Ferrarini, A; Inohara, N; Stamatelopoulos, K; Benguría, A; Cibrian, D; Sánchez-Madrid, F; Alonso-Herranz, V; Dopazo, A; Barbas, C; Vázquez, J; López, JA; González-Martín, A; Nuñez, G; Stellos, K; Bergström, G; Bäckhed, F; Fuster, V; Ibañez, B; Sancho, D
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Affiliations

CIBER Enfermedades Cardiovasc CIBER CV, Madrid, Spain - Author
Ctr Nacl Invest Cardiovasc Carlos III CNIC, Madrid, Spain - Author
German Ctr Cardiovasc Res DZHK, Partner Site Heidelberg Mannheim, Mannheim, Germany - Author
Heidelberg Univ, Helmholtz Inst Translat AngioCardioSci HI TAC, Max Delbruck Ctr Mol Med Helmholtz Assoc MDC, Mannheim, Germany - Author
Heidelberg Univ, Med Fac Mannheim, European Ctr Angioscience ECAS, Dept Cardiovasc Res, Mannheim, Germany - Author
Heidelberg Univ, Univ Med Ctr Mannheim, Dept Med 6, Mannheim, Germany - Author
Hosp La Paz, Inst Hlth Res IdiPAZ, Madrid, Spain - Author
Hosp Univ La Princesa, Inst Invest Sanit, Dept Immunol, Madrid, Spain - Author
Icahn Sch Med Mt Sinai, Zena & Michael A Wiener Cardiovasc Inst, New York, NY USA - Author
Inmunotek SL, Alcala De Henares, Spain - Author
Kings Coll London, Sch Biomed Engn & Imaging Sci, London, England - Author
Mt Sinai Fuster Heart Hosp, Icahn Sch Med Mt Sinai, New York, NY USA - Author
Natl & Kapodistrian Univ Athens Med Sch, Dept Clin Therapeut, Athens, Greece - Author
Osaka Univ, Ctr Infect Dis Educ & Res CIDER, Osaka, Japan - Author
Sahlgrens Univ Hosp, Dept Clin Genet & Genom, Gothenburg, Sweden - Author
Sahlgrens Univ Hosp, Dept Clin Physiol, Gothenburg, Sweden - Author
Tech Univ Denmark, Natl Food Inst, Lyngby, Denmark - Author
Tech Univ Denmark, Novo Nord Fdn Microbiome Hlth Initiat, Lyngby, Denmark - Author
Univ Autonoma Madrid IIS FJD UAM, Fdn Jimenez Diaz, Hlth Res Inst, Madrid, Spain - Author
Univ Autonoma Madrid UAM, Dept Med, Madrid, Spain - Author
Univ Autonoma Madrid, Dept Biochem, Sch Med, Madrid, Spain - Author
Univ Autonoma Madrid, Escuela Doctorado, Madrid, Spain - Author
Univ Autonoma Madrid, Inst Biomed Res Sols Morreale IIBM, Spanish Natl Res Council, Madrid, Spain - Author
Univ Complutense Madrid, Escuela Doctorado, Madrid, Spain - Author
Univ Gothenburg, Dept Mol & Clin Med, Wallenberg Lab, Gothenburg, Sweden - Author
Univ Michigan, Dept Pathol, Med Sch, Ann Arbor, MI USA - Author
Univ Michigan, Med Sch, Rogel Canc Ctr, Ann Arbor, MI USA - Author
Univ Patras, Sch Med, Dept Physiol, Patras, Greece - Author
Univ San Pablo CEU, Fac Farm, Ctr Metabol & Bioanal CEMBIO, CEU Univ, Boadilla Del Monte, Spain - Author
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Abstract

Atherosclerosis is the main underlying cause of cardiovascular diseases. Its prevention is based on the detection and treatment of traditional cardiovascular risk factors1. However, individuals at risk for early vascular disease often remain unidentified2. Recent research has identified new molecules in the pathophysiology of atherosclerosis3, highlighting the need for alternative disease biomarkers and therapeutic targets to improve early diagnosis and therapy efficacy. Here, we observed that imidazole propionate (ImP), produced by microorganisms, is associated with the extent of atherosclerosis in mice and in two independent human cohorts. Furthermore, ImP administration to atherosclerosis-prone mice fed with chow diet was sufficient to induce atherosclerosis without altering the lipid profile, and was linked to activation of both systemic and local innate and adaptive immunity and inflammation. Specifically, we found that ImP caused atherosclerosis through the imidazoline-1 receptor (I1R, also known as nischarin) in myeloid cells. Blocking this ImP-I1R axis inhibited the development of atherosclerosis induced by ImP or high-cholesterol diet in mice. Identification of the strong association of ImP with active atherosclerosis and the contribution of the ImP-I1R axis to disease progression opens new avenues for improving the early diagnosis and personalized therapy of atherosclerosis.
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Keywords

AnimalsAtherosclerosisCohort studiesDiet, high-fatDisease progressionEndothelial-cell functionFemaleGood health and well-beingGutHumansImidazolesInflammationMacrophage mtorMaleMiceMice, inbred c57blMolecular targeted therapyPesaProgressionPropionatesRisSubclinical atherosclerosis

Quality index

Bibliometric impact. Analysis of the contribution and dissemination channel

The work has been published in the journal NATURE due to its progression and the good impact it has achieved in recent years, according to the agency WoS (JCR), it has become a reference in its field. In the year of publication of the work, 2025, it was in position 2/136, thus managing to position itself as a Q1 (Primer Cuartil), in the category Multidisciplinary Sciences. Notably, the journal is positioned above the 90th percentile.

Independientemente del impacto esperado determinado por el canal de difusión, es importante destacar el impacto real observado de la propia aportación.

Según las diferentes agencias de indexación, el número de citas acumuladas por esta publicación hasta la fecha 2026-04-03:

  • WoS: 17
  • Scopus: 14
  • Europe PMC: 11
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Impact and social visibility

From the perspective of influence or social adoption, and based on metrics associated with mentions and interactions provided by agencies specializing in calculating the so-called "Alternative or Social Metrics," we can highlight as of 2026-04-03:

  • The use, from an academic perspective evidenced by the Altmetric agency indicator referring to aggregations made by the personal bibliographic manager Mendeley, gives us a total of: 119.
  • The use of this contribution in bookmarks, code forks, additions to favorite lists for recurrent reading, as well as general views, indicates that someone is using the publication as a basis for their current work. This may be a notable indicator of future more formal and academic citations. This claim is supported by the result of the "Capture" indicator, which yields a total of: 119 (PlumX).

With a more dissemination-oriented intent and targeting more general audiences, we can observe other more global scores such as:

  • The Total Score from Altmetric: 657.
  • The number of mentions on the social network Facebook: 3 (Altmetric).
  • The number of mentions on the social network X (formerly Twitter): 481 (Altmetric).
  • The number of mentions on Wikipedia: 2 (Altmetric).
  • The number of mentions in news outlets: 33 (Altmetric).

It is essential to present evidence supporting full alignment with institutional principles and guidelines on Open Science and the Conservation and Dissemination of Intellectual Heritage. A clear example of this is:

  • The work has been submitted to a journal whose editorial policy allows open Open Access publication.
Continuing with the social impact of the work, it is important to emphasize that, due to its content, it can be assigned to the area of interest of ODS 3 - Ensure healthy lives and promote well-being for all at all ages, with a probability of 57% according to the mBERT algorithm developed by Aurora University.
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Leadership analysis of institutional authors

This work has been carried out with international collaboration, specifically with researchers from: Denmark; Germany; Greece; Japan; Sweden; United Kingdom; United States of America.

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Awards linked to the item

The authors thank M. C. Collado for mouse gut microbiota analysis; M. O. Garmendia for assistance with the metadata from volunteers; members of the D.S. laboratory for help with discussions and critical reading of the manuscript; and the CNIC facilities, foremost the animal, cellomics, histology, metabolomics, genomics, microscopy, clinical trial and bioinformatics facilities, and personnel for assistance. I.R.-V. is funded by FJC2021-048099-I funded by MCIN/AEI/10.13039/501100011033 and European Union NextGenerationEU/PRTR. D.M. is funded by grant PRE2020-092578 MCIN/AEI/10.13039/501100011033. M.G. is funded by beca de formacion de profesorado Universitario fellowship 20/01418. M.F.-M. is funded by INPhINIT Retaining 2024 from Caixa Foundation LCF/BQ/DR24/12080010. A.R.-U. is supported by Community of Madrid (PIPF-2022/SALGL-24581). R.B.-R. is funded by Beca de Formacion de Profesorado Universitario Fellowship 20/03365. A. Devesa is scientifically supported by the Thrasher Research Fund and acknowledges the support of Sociedad Espanola de Cardiologia (grant SEC/PRS-MOV-INT20/002). Work in the D.S. laboratory is funded by the CNIC; the European Union's Horizon 2020 Research and Innovation Program under grant agreement ERC-2016-Consolidator Grant 725091; Ministerio de Ciencia, Innovacion y Universidades (MICIU) PID2022-137712OB-I00, CPP2021-008310 and CPP2022-009762 MICIU/AEI/10.13039/501100011033 Agencia Estatal de Investigacion, Union Europea NextGenerationEU/PRTR; Comunidad de Madrid (P2022/BMD-7333 INMUNOVAR-CM); Scientific Foundation of the Spanish Association Against Cancer (AECC- PRYGN246642SANC); Worldwide Cancer Research WWCR-25-0080; European Union ERC-2023-PoC; a research agreement with Inmunotek S.L.; and la Caixa Foundation (LCF/PR/HR23/52430012 and LCF/PR/HR22/52420019). Work in the B.I. laboratory is supported by the European Commission (H2020-HEALTH 945118 and ERC-CoG 819775); the PID2022-140176OB-I00, PID2019-107332RB-I00 MCIN/AEI /10.13039/501100011033; and the Comunidad de Madrid RENIM P2022/BMD-7403. F.B. is funded by grants from the Swedish Heart Lung Foundation (20240882) and is a Wallenberg Fellow and recipient of an ERC-Advanced grant 2022 (101096705-IMPACT). K. Stellos was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation - Project ID 394046768 - SFB1366 'Vascular control of organ function' C07), the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation programme (MODVASC, grant agreement 759248), the German Centre for Cardiovascular Research (DZHK) and the Helmholtz-Institute for Translational AngioCardioScience (HI-TAC) of the Max Delbruck Center for Molecular Medicine in the Helmholtz Association (MDC) at Heidelberg University, Heidelberg, Germany. Metabolomics Workbench is supported by NIH grant U2C-DK119886 and OT2-OD030544 grants. The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the MICIU and the Pro CNIC Foundation, and is a Severo Ochoa Center of Excellence (CEX2020-001041-S funded by MICIU/AEI /10.13039/501100011033). The PESA study is funded by the CNIC and Santander Bank. This study was partially funded by an intramural grant CNIC-Severo Ochoa to B.I. and D.S.
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