Evidence map›Paper›PMID 41957310›Full record

ArticleNPJ cardiovascular health2026

Scoping review of preclinical and clinical studies on the role of HMGB1 in heart disease.

Shih-Hsuan Mao, Roger Guan-Jie Luo, Carl Lee, Jia-Ling Ruan, Lynn Williams, Alvaro Viñals Guitart, Kat Steiner, James K K Chan, Juan Enrique Berner, Andrew J M Lewis and 2 more

Abstract read
In one paragraph

Article in NPJ cardiovascular health, 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

12 authors.

Shih-Hsuan MaoThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Roger Guan-Jie LuoDepartment of Plastic and Reconstructive Surgery, Chang Gung Memorial Hospital, Linkuo & Chang Gung University College of Medicine, Taoyuan, Taiwan.
Carl LeeThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Jia-Ling RuanDepartment of Oncology, University of Oxford, Oxford, UK.
Lynn WilliamsThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Alvaro Viñals GuitartThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Kat SteinerBodleian Health Care Libraries, University of Oxford, Oxford, UK.
James K K ChanThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Juan Enrique BernerThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK.
Andrew J M LewisOxford Centre for Clinical Magnetic Resonance Research, University of Oxford, Oxford, UK.
Paul R RileyInstitute of Developmental and Regenerative Medicine, University of Oxford, Oxford, UK.
Jagdeep NanchahalThe Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, University of Oxford, Oxford, UK. jagdeep.nanchahal@kennedy.ox.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High Mobility Group Box 1 (HMGB1) is a critical regulator of cardiac injury and repair. However, there is conflicting evidence regarding whether HMGB1 is beneficial or deleterious. We evaluated and synthesised available evidence regarding the molecular functions as well as the clinical and therapeutic utility of HMGB1 in heart disease. We found that overall, the effects depend on the redox state and subcellular location, although most studies failed to identify these parameters clearly. Nuclear upregulation or exogenous administration of fully reduced HMGB1 was beneficial. The partially oxidised form of HMGB1 (dsHMGB1) in the cytoplasm depleted intranuclear HMGB1, and extracellular dsHMGB1 was proinflammatory. Clinically, elevated circulating HMGB1 levels correlate with disease severity and may be a useful prognostic biomarker. Future research should specify the subcellular location and redox state of HMGB1. The development of methods to identify the different redox isoforms would help uncover the therapeutic potential of this multifaceted protein.

Identifiers

PMID41957310
PMCPMC13066481

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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.