Evidence map›Paper›PMID 36655373›Full record

ReviewCardiovascular research2024

Bone marrow inflammatory memory in cardiometabolic disease and inflammatory comorbidities.

Ioannis Mitroulis, George Hajishengallis, Triantafyllos Chavakis

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

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  18. Oral microbiota in cardiovascular health and disease.Frontiers in cellular and infection microbiology · 2025
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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

3 authors at 3 institutions in 4 countries.

Ioannis MitroulisInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine, Technische Universität Dresden, 01307 Dresden, Germany.
George HajishengallisDepartment of Basic and Translational Sciences, Laboratory of Innate Immunity and Inflammation, Penn Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Triantafyllos ChavakisInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine, Technische Universität Dresden, 01307 Dresden, Germany.
Democritus University of Thrace · GRUniversity of Edinburgh · GBUniversity of Pennsylvania · US

Funding

IL-22, Immune Plasticity, and Autotherapy in the PeriodontiumR01DE029436 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2020 to 2024
$1.9M
Trained innate immunity and periodontitis-associated comorbiditiesR01DE031206 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI Georgios Hajishengallis · 2022 to 2026
$1.9M
Aging and dysfunction of progenitor niches: Role of Del-1R01DE028561 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI HAJISHENGALLIS, GEORGIOS · 2020 to 2024
$1.7M
European Research CouncilNIDCR NIH HHS R01 DE028561NIDCR NIH HHS R01 DE029436NIDCR NIH HHS R01 DE031206
6 · The paper itself

Abstract

Cardiometabolic disorders are chief causes of morbidity and mortality, with chronic inflammation playing a crucial role in their pathogenesis. The release of differentiated myeloid cells with elevated pro-inflammatory potential, as a result of maladaptively trained myelopoiesis may be a crucial factor for the perpetuation of inflammation. Several cardiovascular risk factors, including sedentary lifestyle, unhealthy diet, hypercholesterolemia, and hyperglycemia, may modulate bone marrow hematopoietic progenitors, causing sustained functional changes that favour chronic metabolic and vascular inflammation. In the present review, we summarize recent studies that support the function of long-term inflammatory memory in progenitors of the bone marrow for the development and progression of cardiometabolic disease and related inflammatory comorbidities, including periodontitis and arthritis. We also discuss how maladaptive myelopoiesis associated with the presence of mutated hematopoietic clones, as present in clonal hematopoiesis, may accelerate atherosclerosis via increased inflammation.

Indexed as

AtherosclerosisBone MarrowHematopoiesisHematopoietic Stem CellsHumansInflammationMyelopoiesiscardiovascular riskclonal hematopoiesishematopoietic stem and progenitor cellstrained immunity

Identifiers

PMID36655373
PMCPMC10874275
OpenAlexW4317423836

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.