Aging significantly impacts the hematopoietic system, reducing its regenerative capacity and ability to restore homeostasis after stress. Mouse models have been invaluable in studying this process due to their shorter lifespan and the ability to explore genetic, treatment, and environmental influences on aging. However, not all aspects of aging are mirrored between species. This review compares three key aging biomarkers in the hematopoietic systems of mice and humans: myeloid bias, telomere attrition, and epigenetic clocks. Myeloid bias, marked by an increased fraction of myeloid cells and decreased lymphoid cells, is a significant aging marker in mice but is scarcely observed in humans after childhood. Conversely, telomere length is a robust aging biomarker in humans, whereas mice exhibit significantly different telomere dynamics, making telomere length less reliable in the murine system. Epigenetic clocks, based on DNA methylation changes at specific genomic regions, provide precise estimates of chronologic age in both mice and humans. Notably, age-associated regions in mice and humans occur at homologous genomic locations. Epigenetic clocks, depending on the epigenetic signatures used, also capture aspects of biological aging, offering powerful tools to assess genetic and environmental impacts on aging. Taken together, not all blood aging biomarkers are transferable between mice and humans. When using murine models to extrapolate human aging, it may be advantageous to focus on aging phenomena observed in both species. In conclusion, although mouse models offer significant insights, selecting appropriate biomarkers is crucial for translating findings to human aging.
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http://dx.doi.org/10.1016/j.exphem.2024.104600 | DOI Listing |
Virulence
December 2025
Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, Henan, China.
Amino acid metabolism provides significant insight into the development and prevention of many viral diseases. Therefore, the present study aimed to compare the amino acid profiles of hand, foot, and mouth disease (HFMD) patients with those of healthy individuals and to further reveal the molecular mechanisms of HFMD severity. Using UPLC-MS/MS, we determined the plasma amino acid expression profiles of pediatric patients with HFMD (mild, = 42; severe, = 43) and healthy controls ( = 25).
View Article and Find Full Text PDFJ Med Food
December 2024
Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju, Republic of Korea.
Here, we investigated whether a mixture of and (1:3, KGC01CE) could suppress muscle atrophy in HO-induced C2C12 cells and dexamethasone-injected mice. Our results revealed that KGC01CE effectively safeguarded against HO-induced muscle atrophy in C2C12 cells compared with the same mixture at other ratios. We demonstrated that dexamethasone elicited oxidative stress in muscle tissue and decreased the grip strength and cross-sectional areas of muscle fibers; however, oral administration of KGC01CE (1:3) suppressed these dexamethasone-induced changes.
View Article and Find Full Text PDFOcul Immunol Inflamm
December 2024
Department of Ophthalmology, Eye, Ear, Nose, and Throat Hospital of Fudan University, Shanghai, China.
Background: Increased reactive oxygen species (ROS) are involved in the pathological process of dry eye disease. Our previous results suggested that norepinephrine (NE) has a protective effect on dry eye.
Purpose: This study explored the potential therapeutic role and underlying mechanisms of NE in benzalkonium chloride (BAC)-induced dry eye disease.
Clin Transl Med
January 2025
Department of Gynecology, West China Second Hospital, Sichuan University, Chengdu, China.
Background: Hypoxia can affect the occurrence and development of inflammation in humans, but its effects on the disease progression of osteoarthritis (OA) remain unclear. Synovial macrophages play an essential role in the progression of arthritis. Specifically, the activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) in macrophages induces the secretion of a series of inflammatory factors, accelerating the progression of OA.
View Article and Find Full Text PDFClin Transl Med
January 2025
Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Sporadic aortic aneurysm and dissection (AAD) is a critical condition characterised by the progressive loss of vascular smooth muscle cells (VSMCs) and the breakdown of the extracellular matrix. However, the molecular mechanisms responsible for the phenotypic switch and loss of VSMCs in AAD are not fully understood.
Methods And Results: In this study, we employed a discovery-driven, unbiased approach.
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