Clonal hematopoiesis of indeterminate potential and atrial fibrillation DOI
Jie Liu,

Nan Zhang,

Guangshuai Teng

et al.

Heart Rhythm, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Language: Английский

Game changer: Navigating between challenges and hopes in geropharmacology DOI
Qian Chen,

Robert A. Hartman,

Lidia Dankiv

et al.

Advances in pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
TP53 somatic evolution in the normal endometrium of Black and White individuals DOI
Eric Rios‐Doria, Elizabeth U. Parker, Brendan F. Kohrn

et al.

Gynecologic Oncology, Journal Year: 2025, Volume and Issue: 197, P. 1 - 10

Published: April 17, 2025

Language: Английский

Citations

0
Loss of transcriptional factorZbtb33fails to induce clonal hematopoiesis in mice but plays a role in tumor immunity DOI Creative Commons
Yuhang Li,

Kaiping Luo,

Jingjing Liu

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: April 16, 2025

Abstract Clonal hematopoiesis (CH) is an early indicator of hematologic malignancies, driven by mutations in hematopoietic stem cells (HSCs) such as TET2 or TP53. Mutations ZBTB33 have been implicated MDS and suggested a potential driver CH. However, the role its involvement CH remains unclear. We generated Zbtb33 -knockout mouse strain to elucidate immune system. Our findings indicate that -defecient mice appeared grossly normal, competitive bone marrow transplantation assays demonstrated loss HSCs did not confer expansional advantage. Introducing mutation into Tet2 - Tp53 -mutation background yielded no synergistical effects. Tumor challenging influences cancer immunity response, rather than directly driving myeloid malignancies. In summary, deficiency was insufficient induce clonal but may regulatory tumor microenvironment. Statement significance linked cells, To investigate this, we examined function under physiological conditions response external stimuli. Additionally, explored whether cooperate with other genetic drive hematopoiesis. Key points Loss fails does synergize Tet mutations. it plays significant regulating

Language: Английский

Citations

0
Genetic determinants of proteomic aging DOI Creative Commons
Alexander Mörseburg, Yajie Zhao, Katherine A. Kentistou

et al.

npj Aging, Journal Year: 2025, Volume and Issue: 11(1)

Published: April 26, 2025

Abstract Changes in the proteome and its dysregulation have long been known to be a hallmark of aging. We derived proteomic aging trait using data on 1459 plasma proteins from 44,435 UK Biobank individuals measured an antibody-based assay. This metric is strongly associated with four age-related disease outcomes, even after adjusting for chronological age. Survival analysis showed that one-year older age, relative increases all-cause mortality hazard by 13 percent. performed genome-wide association age acceleration (proteomic minus age) identify biological determinants. Proteomic modest genetic correlations epigenetic clocks ( R g = 0.17 0.19) telomere length −0.2). Once we removed associations were explained single pQTL, left three signals mapping BRCA1 , POLR2A TET2 apparent widespread effects Genetic variation at these loci has shown affect other omics-related measures. Mendelian randomisation analyses causal higher BMI type 2 diabetes faster acceleration. supports idea obesity features metabolic syndrome adverse effect processes human

Language: Английский

Citations

0
Clonal hematopoiesis of indeterminate potential and atrial fibrillation DOI
Jie Liu,

Nan Zhang,

Guangshuai Teng

et al.

Heart Rhythm, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Language: Английский

Citations

0