Evidence map›Paper›PMID 39405013›Full record

ReviewGeroScience2025

Genomic instability and genetic heterogeneity in aging: insights from clonal hematopoiesis (CHIP), monoclonal gammopathy (MGUS), and monoclonal B-cell lymphocytosis (MBL).

Attila Kallai, Zoltan Ungvari, Mónika Fekete, Andrea B Maier, Gabor Mikala, Hajnalka Andrikovics, Andrea Lehoczki

Abstract readReview
In one paragraph

Review in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Reversing aging-like 3D genome disorganization in abioRxiv : the preprint server for biology · 2026
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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

7 authors.

Attila KallaiHealthy Aging Program, Institute of Preventive Medicine and Public Health, Semmelweis University, Budapest, Hungary.
Zoltan UngvariVascular Cognitive Impairment, Neurodegeneration and Healthy Brain Aging Program, Department of Neurosurgery, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Mónika FeketeHealthy Aging Program, Institute of Preventive Medicine and Public Health, Semmelweis University, Budapest, Hungary.
Andrea B MaierDepartment of Medicine and Aged Care, @AgeMelbourne, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC, Australia.
Gabor MikalaDoctoral College, Health Sciences Program, Semmelweis University, Budapest, Hungary.
Hajnalka AndrikovicsHealthy Aging Program, Institute of Preventive Medicine and Public Health, Semmelweis University, Budapest, Hungary.
Andrea LehoczkiHealthy Aging Program, Institute of Preventive Medicine and Public Health, Semmelweis University, Budapest, Hungary. Andrea.M.Lehoczki@gmail.com.ORCID 0000-0002-4285-7518

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a multifaceted process characterized by a gradual decline in physiological function and increased susceptibility to a range of chronic diseases. Among the molecular and cellular mechanisms driving aging, genomic instability is a fundamental hallmark, contributing to increased mutation load and genetic heterogeneity within cellular populations. This review explores the role of genomic instability and genetic heterogeneity in aging in the hematopoietic system, with a particular focus on clonal hematopoiesis of indeterminate potential (CHIP), monoclonal gammopathy of undetermined significance (MGUS), and monoclonal B-cell lymphocytosis (MBL) as biomarkers. CHIP involves the clonal expansion of hematopoietic stem cells with somatic mutations. In contrast, MGUS is characterized by the presence of clonal plasma cells producing monoclonal immunoglobulins, while MBL is characterized by clonal proliferation of B cells. These conditions are prevalent in the aging population and serve as measurable indicators of underlying genomic instability. Studying these entities offers valuable insights into the mechanisms by which somatic mutations accumulate and drive clonal evolution in the hematopoietic system, providing a deeper understanding of how aging impacts cellular and tissue homeostasis. In summary, the hematopoietic system serves as a powerful model for investigating the interplay between genomic instability and aging. Incorporating age-related hematological conditions into aging research, alongside other biomarkers such as epigenetic clocks, can enhance the precision and predictive power of biological age assessments. These biomarkers provide a comprehensive view of the aging process, facilitating the early detection of age-related diseases and hopefully enabling personalized healthcare strategies.

Indexed as

AgingClonal HematopoiesisGenetic HeterogeneityGenomic InstabilityLymphocytosisMonoclonal Gammopathy of Undetermined SignificanceParaproteinemiasB-LymphocytesHumansMutationAgingBiological ageBiomarkerClockMutation

Identifiers

PMID39405013
PMCPMC11872960

What Socratic 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 Socratic graph.