One of the proposed mechanisms linking childhood stressor exposure to negative mental and physical health outcomes in later life is cellular aging. In this prospective, longitudinal, and pre-registered study, we examined the association between a cumulative pattern of childhood risk exposure from age 6 to age 10 (i.e., poor maternal mental health, parental relationship problems, family/friend death, bullying victimization, poor quality friendships) and change in two biomarkers of cellular aging (i.e., telomere length, epigenetic age) from age 6 to age 10 in a Dutch low-risk community sample (n = 193). We further examined the moderating effect of cortisol reactivity at age 6. Ordinary Least Squares regression analyses revealed no significant main effects of childhood risk exposure on change in cellular aging, nor a moderation effect of child cortisol reactivity. Secondary findings showed a positive correlation between telomere length and cortisol reactivity at age 6, warranting further investigation. More research in similar communities is needed before drawing strong conclusions based on the null results.
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http://dx.doi.org/10.1111/psyp.14205 | DOI Listing |
Biogerontology
December 2024
Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China.
Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases.
View Article and Find Full Text PDFJ Funct Biomater
December 2024
Cardiovascular Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
Reactive oxygen species (ROS) are generated predominantly during cellular respiration and play a significant role in signaling within the cell and between cells. However, excessive accumulation of ROS can lead to cellular dysfunction, disease progression, and apoptosis that can lead to organ dysfunction. To overcome the short half-life of ROS and the relatively small amount produced, various imaging methods have been developed, using both endogenous and exogenous means to monitor ROS in disease settings.
View Article and Find Full Text PDFCurr Issues Mol Biol
December 2024
The First College of Clinical Medicine, Lanzhou University, Lanzhou 730000, China.
The Y-box binding protein 1 (YBX1) is a multifunctional protein with a wide range of roles in cell biology. It plays a crucial role in immune modulation, senescence, and disease progression. This review presents a comprehensive analysis of the specific functions and mechanisms of YBX1 in these areas.
View Article and Find Full Text PDFCurr Issues Mol Biol
December 2024
Department of Biophysics, Institute of Biology and Biomedicine, Lobachevsky State University of Nizhny Novgorod, 23 Gagarin Ave., 603022 Nizhny Novgorod, Russia.
Modern radiotherapy utilizes a broad range of sources of ionizing radiation, both low-dose-rate (LDR) and high-dose-rate (HDR). However, the mechanisms underlying specific dose-rate effects remain unclear, especially for corpuscular radiation. To address this issue, we have irradiated human epidermoid carcinoma A431 cells under LDR and HDR regimes.
View Article and Find Full Text PDFCurr Issues Mol Biol
December 2024
Department of Pharmacology and Public Health, Faculty of Medicine, The Hashemite University, Zarqa 13133, Jordan.
Oncogene-induced senescence (OIS) is a form of cellular senescence triggered by oncogenic signaling and, potentially, by infection with oncogenic viruses. The role of senescence, along with its associated secretory phenotype, in the development of cervical cancer remains unclear. Additionally, the expression of the senescence-associated secretory phenotype (SASP) has not yet been explored in cervical premalignant lesions infected by the Human Papilloma Virus (HPV).
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