ArticleFrontiers in neurology
Subtype-specific effects of clonal hematopoiesis on cerebrovascular and cardiometabolic disease risk.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cerebrovascular and related cardiometabolic diseases frequently cluster in aging populations characterized by metabolic dysfunction and chronic inflammation. Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as an age-related modifier associated with inflammation, metabolic disturbance, and vascular risk. However, whether CHIP exerts subtype-specific effects on cerebrovascular outcomes within a broader cardiometabolic context remains incompletely understood. Objectives: This study aimed to investigate the causal associations of CHIP and its major genetic subtypes with cerebrovascular and cardiovascular diseases, while examining cancer outcomes as broader systemic context. Methods: We performed Mendelian randomization analyses of overall CHIP and its five subtypes (DNMT3A, TET2, JAK2, TP53, and ASXL1) in relation to 20 cerebrovascular and cardiovascular diseases and 19 site-specific cancers. Complementary in vitro experiments were conducted to validate the biological contribution of the key subtype under inflammatory and metabolic stress conditions. Results: Genetically predicted CHIP showed marked heterogeneity across cerebrovascular and cardiovascular outcomes. Among the CHIP subtypes, TET2-CHIP showed the clearest cerebrovascular signal, with significant associations with ischemic stroke, intracerebral hemorrhage, and hypertension. ASXL1-CHIP also showed directional risk elevations for intracerebral hemorrhage and hypertension. In contrast, JAK2-CHIP exhibited inverse associations with intracerebral hemorrhage and atrial fibrillation, whereas DNMT3A-CHIP was positively associated with atrial fibrillation and inversely associated with abdominal aortic aneurysm. Cancer analyses showed additional subtype-specific associations across disease outcomes. Experimental studies further showed that Conclusions: CHIP is associated with subtype-specific patterns of cerebrovascular risk within a broader cardiometabolic context. TET2-CHIP showed the most consistent associations with cerebrovascular outcomes. The marked heterogeneity across CHIP subtypes indicates that clonal hematopoiesis should not be considered a uniform exposure, but rather a mutation-defined condition with distinct clinical consequences.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.