Review
Cell Biology
Claire Ghilain, Eric Gilson, Marie-Josephe Giraud-Panis
Summary: Protecting telomeres from the DNA damage response is crucial to prevent cellular senescence and aging; telomere DNA shortening in dividing somatic cells leads to replicative senescence, contributing to aging; the Shelterin protein complex plays a key role in protecting telomeres and its changes in structure and function during development and aging are a subject of intense research.
Review
Cell Biology
Ashish Kumar, Kavitha Thirumurugan
Summary: Normal somatic cells undergo finite cellular divisions, but they can be arrested in response to various stressors such as oxidative stress, oncogene-induced abnormalities, genotoxic stress, and telomere attrition. Repair mechanisms are activated during the cell cycle pause caused by stress, and the nature of the stress determines whether repair or permanent arrest occurs. Quiescence allows damaged cells to repair and return to the cell cycle, while senescence is irreversible and leads to age-related disorders.
Review
Biochemistry & Molecular Biology
Jamil Nehme, Abdullah Altulea, Teodora Gheorghe, Marco Demaria
Summary: Evidence suggests that metabolism is a major regulator of aging and that dietary interventions and metabolic perturbations can extend health and lifespan. A common target for delaying aging is cellular senescence, which involves growth arrest and the activation of pro-inflammatory factors. This article summarizes current knowledge on carbohydrate, lipid, and protein metabolism and their role in regulating cellular senescence. It also discusses the potential of dietary interventions to prevent disease and extend healthy longevity by modulating senescence-associated phenotypes, and the need for personalized nutritional interventions based on individual health and age status.
BIOMEDICAL JOURNAL
(2023)
Article
Cell Biology
Ying Ao, Zhuping Wu, Zhiwei Liao, Juncong Lan, Jie Zhang, Pengfei Sun, Baohua Liu, Zimei Wang
Summary: The nuclear matrix protein lamin A plays multiple roles in the cell, including DNA replication and repair, gene activation, transcriptional regulation, and maintenance of chromatin structure. Phosphorylation of lamin A determines its mobility in the nucleus and nuclear membrane dissolution. This study investigates the regulation of lamin A phosphorylation during interphase and demonstrates that C-terminal mutations can induce cellular senescence. The results suggest that phosphorylation at specific C-terminal sites is crucial for genomic stability and prevention of cellular senescence.
Review
Cell Biology
Lidya Kristiani, Youngjo Kim
Summary: Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the ability of cells to neutralize them. This can lead to cellular damage, including DNA damage and cellular senescence. The nuclear lamina (NL), which provides structure to the nucleus, is affected by oxidative stress, resulting in dysregulation of gene expression and age-related diseases. Understanding the interplay between oxidative stress and the NL is crucial for developing treatments for related diseases.
Article
Biochemistry & Molecular Biology
Deniz Karabag, Hannah Scheiblich, Angelika Griep, Francesco Santarelli, Stephanie Schwartz, Michael T. Heneka, Christina Ising
Summary: The highest risk factor for the development of tauopathies is aging. Senescent microglia have been identified in the brains of tau-transgenic mice and patients suffering from tauopathies. Exposure to tau can lead to microglial senescence, suggesting the presence of a vicious circle.
JOURNAL OF NEUROCHEMISTRY
(2023)
Article
Endocrinology & Metabolism
Davis A. Englund, Alyssa Jolliffe, Zaira Aversa, Xu Zhang, Ines Sturmlechner, Ayumi E. Sakamoto, Julianna D. Zeidler, Gina M. Warner, Colton McNinch, Thomas A. White, Eduardo N. Chini, Darren J. Baker, Jan M. van Deursen, Nathan K. LeBrasseur
Summary: Recent research has found associations between elevated levels of p21, the accumulation of senescent cells, and skeletal muscle dysfunction in mice and humans. By using a mouse model with p21 overexpression, the study investigated the role of p21 in cellular senescence and pathological features in skeletal muscle. The findings showed that p21 induced several characteristic features of cellular senescence in skeletal muscle, including altered gene expression, DNA damage, mitochondrial dysfunction, and the senescence-associated secretory phenotype. Additionally, the p21OE mice exhibited skeletal muscle pathology, such as atrophy, fibrosis, and impaired physical function, highlighting p21 as a driver of cellular senescence and a new source of skeletal muscle loss and dysfunction.
MOLECULAR METABOLISM
(2023)
Article
Cell Biology
Miriam Bobadilla Munoz, Josune Orbe, Gloria Abizanda, Florencio J. D. Machado, Amaia Vilas, Asier Ullate-Agote, Leire Extramiana, Arantxa Baraibar Churio, Xabier L. Aranguren, Gloria Cantero, Neira Sainz Amillo, Jose Antonio Rodriguez, Luis Ramos Garcia, Juan Pablo Romero Riojas, Ainara Vallejo-Illarramendi, Carmen Paradas, Adolfo Lopez de Munain, Jose Antonio Paramo, Felipe Prosper, Ana Perez-Ruiz
Summary: Aged muscles have a decline in their response to damage, which is mainly attributed to intrinsic defects in satellite cells. However, changes in the muscle-stem cell microenvironment also contribute to aging. Loss of MMP-10 in young mice alters the muscle ECM and disrupts the satellite cell niche, leading to premature aging features. MMP-10 has a protective effect on satellite cells and can delay their aging and overcome dysfunction in muscular dystrophy.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2023)
Review
Immunology
Lilian R. Polsky, Kelly E. Rentscher, Judith E. Carroll
Summary: Exposure to chronic adverse conditions and the resulting neurobiological response may increase the risk of early onset of age-related diseases and accelerate biological aging. The mechanisms through which chronic psychosocial stress influences distinct biological aging pathways likely involve multiple layers in the physiological-molecular network. This review integrates research using animal, human, and in vitro models to explore the pathways and neuroendocrine mediators involved.
BRAIN BEHAVIOR AND IMMUNITY
(2022)
Article
Cell Biology
Chin Yee Ho, Oliver Dreesen
Summary: Skin is composed of different cell types with varying proliferative capacities, and aging occurs due to both chronological factors and exposure to external stimuli. The accumulation of senescent cells in different skin compartments during aging can lead to impaired skin physiology. The specific mechanisms by which different skin cell types respond to senescence-inducing stimuli and contribute to aging-related skin phenotypes and pathologies remain unclear.
MECHANISMS OF AGEING AND DEVELOPMENT
(2021)
Article
Geriatrics & Gerontology
Cara L. Green, Davis A. Englund, Srijit Das, Mariana M. Herrerias, Matthew J. Yousefzadeh, Rogan A. Grant, Josef Clark, Heidi H. Pak, Peiduo Liu, Hua Bai, Veena Prahlad, Dudley W. Lamming, Daniella E. Chusyd
Summary: This report summarizes cutting-edge research covered in a virtual symposium held by the 2021 Midwest Aging Consortium, highlighting various topics related to aging and health across common laboratory animals and less-common species. The consensus among symposium speakers is the strength of aging research in the Midwestern United States and the benefits of a collaborative and diverse approach to geroscience.
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
(2021)
Article
Cell Biology
Anda Huna, Audrey Griveau, David Vindrieux, Sara Jaber, Jean-Michel Flaman, Delphine Goehrig, Lamia Azzi, Jean-Jacques Medard, Sophia Djebali, Hector Hernandez-Vargas, Robert Dante, Lea Payen, Jacqueline Marvel, Philippe Bertolino, Sebastien Aubert, Pierre Dubus, David Bernard
Summary: The study reveals that PLA2R1 suppresses aging-induced tumors by repressing PARP1 expression and inducing DNA damage. Mechanistically, PLA2R1 represses PARP1 via a ROS-Rb signaling axis, leading to DNA damage and tumor suppressive responses in cells.
CELL DEATH & DISEASE
(2021)
Article
Chemistry, Multidisciplinary
Yangjing Zhao, Xia Liu, Fusheng Si, Lan Huang, Aiqin Gao, Wenli Lin, Daniel F. Hoft, Qixiang Shao, Guangyong Peng
Summary: Citrate treatment suppresses tumor cell proliferation by promoting lipid biosynthesis and disrupting lipid metabolism, inducing cell senescence and growth inhibition. Targeting citrate can be a promising therapeutic strategy for tumor treatment.
Article
Biochemistry & Molecular Biology
Jiongbiao Zhong, Joseph Chen, Anthony A. Oyekan, Michael W. Epperly, Joel S. Greenberger, Joon Y. Lee, Gwendolyn A. Sowa, Nam V. Vo
Summary: This study investigates the effects of ionizing radiation on cellular senescence and matrix catabolism in the annulus fibrosus. The results suggest that radiation-induced cellular senescence can contribute to matrix degradation, which may have adverse effects on spinal health.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Stuart Maudsley, Claudia Schrauwen, Irem Harputluoglu, Deborah Walter, Hanne Leysen, Patricia McDonald
Summary: This study identified G protein-coupled receptor 19 (GPR19) as a pseudo-orphan GPCR that is sensitive to various molecular aspects of aging. The functionality of GPR19 is specifically associated with sensory, protective, and remedial signaling systems related to aging-related pathology. GPR19 may act as a coordinator of aging-associated metabolic dysfunction, stress response, DNA integrity management, and cellular senescence.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
