bims-minfam 2025-05-25 papers

Protein Cell. 2025 May 20. pii: pwaf031. [Epub ahead of print]

Correction to: SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer.

DOI: https://doi.org/10.1093/procel/pwaf031

Nat Med. 2025 May 16.

Using metformin to stall clonal hematopoiesis.

Karen O'Leary.

Keywords: Haematological diseases; Metabolism; Translational research

DOI: https://doi.org/10.1038/d41591-025-00032-w

Nat Aging. 2025 May 23.

Aberrant engagement of P-selectin drives hematopoietic stem cell aging in mice.

Daozheng Yang, Natalia Skinder, Yun-Ruei Kao, Jiahao Chen, Victor Thiruthuvanathan, Arthur Flohr Svendsen, Chi Zhang, Bertien Dethmers-Ausema, Ellen Weersing, Maria Maryanovich, Britta Will, Gerald de Haan.

During aging, hematopoietic stem cell (HSC) function progressively declines which can lead to reduced blood cell production and regeneration. This work uncovered that cell surface presentation of P-selectin (CD62P, encoded by Selp) increases in a large fraction of aging HSCs driven by a proinflammatory milieu in mice. Notably, expression of P-selectin molecularly and functionally dichotomized the aging HSC pool; stem cells presenting with highly abundant P-selectin were hallmarked by aging-associated gene expression programs and reduced repopulation capacity upon regenerative stress. Ectopic expression of Selp in young HSCs was sufficient to impair long-term reconstitution potential and impair erythropoiesis. Mechanistically, we uncovered that P-selectin receptor activation by its primary ligand, P-selectin glycoprotein ligand-1, suppressed aging-associated gene expression, and, reversely, lack of P-selectin signaling led to HSC premature aging. Collectively, our study uncovered a functional role of P-selectin engagement in regulating HSC regeneration and driving stem cell aging when perturbed.

DOI: https://doi.org/10.1038/s43587-025-00880-8

Nat Aging. 2025 May 20.

GLP-1R agonists protect against Alzheimer's disease by rewiring energy regulation.

Daxiang Na, Marc Schneeberger Pané.

DOI: https://doi.org/10.1038/s43587-025-00881-7

Cancer Sci. 2025 May 19.

Clonal Hematopoiesis and Solid Cancers.

Yen T M Nguyen, Manabu Fujisawa, Shumpei Ishikawa, Mamiko Sakata-Yanagimoto.

Clonal hematopoiesis refers to the expansion of hematopoietic stem cells harboring somatic mutations, a phenomenon increasingly recognized in aging populations. This review highlights the emerging relationship between clonal hematopoiesis and solid cancers, focusing on the prevalence and impact of clonal hematopoiesis-associated mutations such as DNMT3A, TET2, ASXL1, and TP53 in tumorigenesis. Key risk factors for the co-occurrence of clonal hematopoiesis and solid cancers, including germline genetic factors, aging, and environmental factors, are also discussed. We explore how clonal hematopoiesis mutations shape the tumor microenvironments in solid cancers by modulating immunoregulation, inflammation, and angiogenesis, thereby contributing to tumor progression. These findings underscore the dual role of clonal hematopoiesis as both a marker of cancer risk and a potential driver of solid cancer progression. The clinical implications of clonal hematopoiesis are also considered, including the prognostic value, impact on treatment response, and potential as a therapeutic target. Future directions are outlined to advance our understanding of clonal hematopoiesis and to exploit its clinical potential for cancer management.

Keywords: TET2 mutations; T‐cell lymphomas; aging; clonal hematopoiesis; solid cancers; tumor microenvironments

DOI: https://doi.org/10.1111/cas.70097