Evidence map›Paper›PMID 30306212›Full record

ReviewCellular and molecular life sciences : CMLS2019

The Janus face of HMGB1 in heart disease: a necessary update.

Angela Raucci, Stefania Di Maggio, Francesco Scavello, Alessandro D'Ambrosio, Marco E Bianchi, Maurizio C Capogrossi

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% of its field
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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
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  9. TIM-3 in Cardiovascular Disease.Current heart failure reports · 2026
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19 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Angela RaucciUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy. araucci@ccfm.it.
Stefania Di MaggioUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy.
Francesco ScavelloUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy.
Alessandro D'AmbrosioUnit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy.
Marco E BianchiChromatin Dynamics Unit, Università Vita-Salute San Raffaele, Milan, Italy.
Maurizio C CapogrossiDepartment of Cardiology, Ochsner Medical Center, New Orleans, USA.
Centro Cardiologico Monzino · ITJohns Hopkins Bayview Medical Center · USVita-Salute San Raffaele University · IT

Funding

Centro Cardiologico Monzino Ricerca Corrente 2017-2018Fondazione Cariplo Research on Ageing diseases 2015Fondazione IEO-Monzino Fellowship 2017
6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein involved in transcription regulation, DNA replication and repair and nucleosome assembly. HMGB1 is passively released by necrotic tissues or actively secreted by stressed cells. Extracellular HMGB1 acts as a damage-associated molecular pattern (DAMPs) molecule and gives rise to several redox forms that by binding to different receptors and interactors promote a variety of cellular responses, including tissue inflammation or regeneration. Inhibition of extracellular HMGB1 in experimental models of myocardial ischemia/reperfusion injury, myocarditis, cardiomyopathies induced by mechanical stress, diabetes, bacterial infection or chemotherapeutic drugs reduces inflammation and is protective. In contrast, administration of HMGB1 after myocardial infarction induced by permanent coronary artery ligation ameliorates cardiac performance by promoting tissue regeneration. HMGB1 decreases contractility and induces hypertrophy and apoptosis in cardiomyocytes, stimulates cardiac fibroblast activities, and promotes cardiac stem cell proliferation and differentiation. Interestingly, maintenance of appropriate nuclear HMGB1 levels protects cardiomyocytes from apoptosis by preventing DNA oxidative stress, and mice with HMGB1cardiomyocyte-specific overexpression are partially protected from cardiac damage. Finally, higher levels of circulating HMGB1 are associated to human heart diseases. Hence, during cardiac injury, HMGB1 elicits both harmful and beneficial responses that may in part depend on the generation and stability of the diverse redox forms, whose specific functions in this context remain mostly unexplored. This review summarizes recent findings on HMGB1 biology and heart dysfunctions and discusses the therapeutic potential of modulating its expression, localization, and oxidative-dependent activities.

Indexed as

AlarminsAnimalsBiomarkersHeart DiseasesHMGB1 ProteinHumansMyocardial InfarctionMyocarditisOxidative StressReactive Oxygen SpeciesAlarminsBiomarkersHMGB1 ProteinReactive Oxygen SpeciesAlarminBiomarkerInflammationOxidative stressRegeneration

Identifiers

PMID30306212
PMCPMC6339675
OpenAlexW2897423402

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.