Evidence map›Paper›PMID 36214849›Full record

ReviewInnere Medizin (Heidelberg, Germany)2022

[Influence of clonal hematopoiesis on non-hematological diseases and aging processes].

Michael A Rieger

Abstract readEnglish AbstractReview
In one paragraph

Review in Innere Medizin (Heidelberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Michael A RiegerMedizinische Klinik 2, Hämatologie/Onkologie, Klinikum der Goethe-Universität, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Deutschland. m.rieger@em.uni-frankfurt.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The occurrence of clonal hematopoiesis, caused by acquired somatic mutations of leukemia-associated genes in blood stem cells is very common in the population and increases with age. Besides an increased risk of developing myeloid neoplasms, an unexpected causal relationship between clonal hematopoiesis and cardiovascular diseases was recently discovered. Clonal hematopoiesis presents as a new independent and strong risk factor for cardiovascular diseases, such as atherosclerosis, coronary heart disease, heart failure, aortic valve stenosis and stroke, which from a medical perspective should no longer be ignored. Worldwide intensive research for associations of clonal hematopoiesis with other age-related and infectious diseases identifies increasingly more illnesses that are influenced by the presence of mutated blood cells. Current data describe a fatal vicious circle, initiated by somatic blood cell mutations, which accelerate the progression of associated diseases in a proinflammatory way and feed-back to hematopoiesis leading to a further enlargement of the mutated blood cell clone. First experimental treatment approaches to break this vicious circle are discussed here. The causal relationship and the underlying pathomechanisms are now at the center of research interest in order to rapidly establish risk stratification and therapeutic measures for the benefit of patients in the near future.

Indexed as

Cardiovascular DiseasesClonal HematopoiesisAgingHematopoiesisHumansMutationAortic valve stenosisAtherosclerosisCardiovascular diseasesHeart failurePulmonary disease, chronic obstructive

Identifiers

PMID36214849
PMCPMC9549812

What OpenQuestion holds

Textmetadata
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.