Articles tagged with Cellular Senescence
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Researchers have characterized the association between cellular senescence and human brain structure in both development and late life. The study found that senescence-related gene expression is linked to brain volume and cortical organization, with distinct roles depending on cell type and stage of life.
Researchers found that mitochondrial RNA can leak into healthy tissue, triggering inflammation and scarring. Inhibiting certain proteins enables mitochondrial RNA to escape, leading to less inflammation and healthier liver tissue.
Researchers found that glycation stress, caused by methylglyoxal, promotes aortic stiffening and cellular senescence. Natural compound Gly-Low, containing nicotinamide and alpha-lipoic acid, reversed these effects and reduced stiffness in aging mice.
Researchers at Cold Spring Harbor Laboratory have devised a new approach to stimulate cell growth and repair in the intestine using CAR T-cell therapy. This therapy has shown promising results in improving gut health in both young and old mice, with significant reductions in inflammation and improved nutrient absorption.
Researchers explore the link between senescent cells and metabolic diseases, highlighting potential treatments known as senotherapeutics. Senolytics, senomorphics, and senosensitizers are interventions aimed at eliminating or suppressing senescent cells to mitigate metabolic disease.
Researchers at Mayo Clinic have developed a new technique to identify senescent cells using aptamers, which can potentially lead to targeted therapies. The study found several rare aptamers that bind specifically to fibronectin on the surface of mouse cells, offering a promising approach for characterizing and treating senescent cells.
Researchers found that overactive Runx1 gene accelerates age-related degeneration of intervertebral discs, causing premature cellular aging and unhealthy tissue changes. Targeting Runx1 may be a promising strategy to prevent or slow disc aging.
Researchers have discovered that activating lysosome biogenesis alleviates senescence in Hutchinson-Gilford progeria syndrome. By promoting progerin clearance, this approach shows promise as a potential therapeutic avenue for HGPS and other age-related disorders.
A groundbreaking study by Florida Atlantic University researchers found that working with service dogs can slow cellular aging in female veterans. The study, which involved female veterans with post-traumatic stress disorder, revealed promising biological benefits associated with service dog training.
Researchers found that cells exiting the cell cycle show stronger signs of senescence and are more sensitive to senolytic drugs. DNA content plays a crucial role in how aging cells function and respond to treatment.
Researchers found that polyamines primarily activate glycolysis in cancer cells, upregulating eIF5A2 and five ribosomal proteins associated with cancer malignancy. In contrast, eIF5A1 promotes healthy aging by activating mitochondria via autophagy.
A keto diet may have different effects on males and females, with estrogen found to promote protection against adverse effects such as cellular senescence. The study found that male mice on a keto diet showed increased markers of oxidative stress and cellular senescence, but these effects were reversed by estrogen treatment.
Cancer cells with abundant circular DNA elements (ecDNA) carrying oncogenes like MYCN are resistant to chemotherapy. Combining standard chemotherapy with a secondary therapy targeting these senescent cells leads to improved outcomes in mouse models of neuroblastoma and medulloblastoma.
The Aging (Aging-US) meeting will bring together researchers and clinicians to explore the latest advances in cellular senescence and its translation into therapies for age-related diseases. The event will provide a unique platform for discussing both basic research and its clinical applications.
The UT Health San Antonio research team, led by Blake Rasmussen, has been selected as a semifinalist in the XPRIZE Healthspan competition. They will use a low-frequency ultrasound spa to develop a non-invasive treatment that helps renew cells and tissues, potentially improving overall health and longevity.
A new study reveals an AI-assisted technique that can measure and track aging cells, which are known to play a key role in wound repair and aging-related diseases. The tool uses nuclear morphometrics to analyze cell characteristics and distinguish between healthy and senescent cells.
Researchers induced senescence in worms by manipulating transcription factor TFEB, mimicking mammalian aging. Key growth factors insulin and TGFbeta were identified as crucial signaling molecules in circumventing senescence.
Researchers at the University of Oklahoma investigate the overlap between cognitive decline caused by chemotherapy and aging, discovering decreased blood flow, disrupted blood-brain barriers, and senescent cells. Removing these cells with senolytics can improve cerebral blood flow, cognition, and overall brain health.
A Korean research team discovered that High Mobility Group Box 1 (HMGB1) plays a critical role in transmitting senescence from aging cells to distant tissues through the bloodstream. Reduced HMGB1 circulates systemically, inducing senescence in remote tissues and impairing regenerative capacity.
Scientists have created a novel method to distinguish between healthy and senescent cells using electric fields, marking a fresh start in ageing research. The frequency-modulated dielectrophoresis (FM-DEP) technique is label-free, rapid, and easy to apply, allowing for the characterization of cell type by measuring the cutoff frequency.
Scientists at San Raffaele Telethon Institute for Gene Therapy discovered that CRISPR-Cas9 gene editing can cause inflammation and senescence-like responses in blood stem cells. This reduces the cells' ability to regenerate blood cells after transplantation, limiting the long-term success of gene therapy.
Researchers found that surgery induces accumulation of senescent cells in the hippocampal region of aged mice, leading to neuroinflammation. Dosing with a combination of Dasatinib and Quercetin reduced surgery-induced inflammation.
Researchers will examine the link between cellular senescence and Parkinson's disease onset and progression. The team aims to find new ways to slow disease progression and establish senescence as a novel target for treatment.
Research highlights the interconnected relationship between aging, circadian rhythms, and cancer, with shared mechanisms including genomic instability, cellular senescence, and chronic inflammation. Modulating circadian rhythms may serve as a novel strategy to intervene in age-related functional decline and treat cancer.
A newly discovered mechanism has identified a key protein, AP2A1, that toggles between 'young' and 'old' cell states. By suppressing AP2A1 in older cells, researchers were able to reverse senescence and promote cellular rejuvenation. This breakthrough may lead to new treatment targets for diseases associated with old age.
A new study from Penn State finds that oral tissue samples significantly affect epigenetic clock accuracy, leading to older age estimates. Researchers tested five tissue types and seven epigenetic clocks, concluding that blood-based samples are more accurate in measuring biological age.
A review of cell death and aging in cancer research reveals the significance of cellular senescence in promoting cancer growth. The study highlights the potential of various types of programmed cell death, such as necroptosis and pyroptosis, as therapeutic targets against senescent cells.
Researchers discovered that removing arginase-II gene can slow down muscle aging in mice, leading to improved muscle health and reduced inflammation. This finding suggests targeting the Arg-II gene could help maintain muscle strength and mobility in older adults.
Regular aerobic exercise has been shown to significantly reduce disease markers associated with Alzheimer's, protecting healthy brain cells and restoring balance in the aging brain. The study highlights the potential for aerobic exercise to serve as a cornerstone in preventive strategies for Alzheimer's.
Researchers will explore the role of exosomes in delivering regenerative compounds, while also investigating olfactory receptors' unexpected functions in skin health. The conference aims to slow or reverse skin aging through novel approaches to mitochondrial function and microbiota balance.
Researchers used a mouse model to assess the impact of senolytic agents dasatinib and quercetin on pelvic organ prolapse. The study found that D+Q injections did not result in significant differences in prolapse development but reduced cellular senescence markers.
Polyploidy, a state with extra genetic material, allows cancer cells to survive longer under DNA damage. This phenomenon explains why some cancers are resistant to anti-cancer drug treatments.
Researchers investigate how liver necroptosis triggers inflammation in both organs, leading to cognitive impairment. Studying aging mouse models, they found that liver necroptosis causes systemic inflammation affecting brain function.
A new study found that common breast cancer treatments, including chemotherapy, radiation, and surgery, can increase expression of aging markers in breast cancer survivors. The study suggests that these treatments can have a more extensive impact on the body than previously thought, leading to accelerated biological aging.
Researchers found high prevalence of frailty in breast cancer and hematopoietic cell transplant survivors, negatively impacting physical functioning and quality of life. The study supports an association between frailty and the senescence marker p16INK4a, highlighting the need for well-designed senolytic trials.
Researchers have developed an AI technology that can analyze mammary tissue biopsies to identify signs of damaged cells, a key indicator of breast cancer risk. The study found the AI was far better at predicting risk than current clinical benchmarks, offering improved treatment options for women.
Research published in Nature Aging has shown that deleting the S6K1 gene in aged mouse livers reduces inflammation by suppressing inflammatory protein production, linking metabolic regulation to aging and disease. This finding provides a biological mechanism for the beneficial effects of removing S6K1 on health span.
Researchers found that artificial induction of GluCer leads to cellular senescence in DA neurons, highlighting the role of lipid aggregation in PD. The study proposes that lysosomal impairment and lipid accumulation trigger expression of a cellular senescence phenotype in vulnerable DA neurons.
Researchers created a new cell model to study the effects of senescence on lung fibroblasts. Senescent alveolar epithelial cells triggered fibrotic activation in lung fibroblasts, which was attenuated by senolytic therapy.
The study found that exercise increased PEDF levels in skeletal muscles and suppressed senescence markers in the lungs. PEDF also reduced senescence markers in multiple tissues and attenuated decline in respiratory function in pulmonary emphysema mouse model, suggesting its potential as a therapeutic agent for age-related diseases.
A team of scientists from Max Planck Institute found that extremely long-lived proteins in the ovary play a crucial role in preserving fertility. These proteins, known as chaperones, help maintain cellular processes and prevent misfolded proteins from aggregating.
A research team from Osaka University identified a key osteoporosis-related gene, Men1, and developed a new animal model of the disease. The study found that inactivation of Men1 led to cellular senescence in osteoblasts, reducing bone formation activity and increasing bone resorption.
Recent research reveals that targeting senescent cells as the cause of aging is not accurate. Instead, these cells have positive health impacts and may pose risks if targeted therapeutically.
A new review paper explores the mechanistic links between peripheral vascular dysfunction, cerebral vascular dysfunction, and reduced brain health with aging. The study suggests that targeting fundamental aging mechanisms may be a promising strategy to reduce dementia risk.
Weo electrolyzed water (WEW) has been shown to attenuate cellular senescence in both normal fibroblasts and breast cancer cells. The study found that WEW modulated markers of cellular senescence, inflammation, and stress response genes in a cell type-dependent manner.
A new study led by UT Health San Antonio found that long-term ketogenic diets can induce senescence, or aged cells, in normal tissues, affecting heart and kidney function. However, an intermittent ketogenic diet regimen eliminated these pro-inflammatory effects.
Researchers found that ~60% of tissues exhibit a significant negative correlation between age and stemness score, indicating a pan-tissue decline in stemness. This study adds weight to the idea that stem cell deterioration contributes to human aging, with hematopoietic stem cells from older individuals showing higher stemness scores.
Researchers have discovered that PR55α, a regulatory subunit of PP2A phosphatase, inhibits p16 expression and blocks cellular senescence induction by γ-irradiation. This finding provides a new insight into the regulation of the p16/RB pathway in response to stressors.
Researchers investigated the impact of senolytic treatments on DNA methylation clocks and epigenetic age. Results showed significant increases in epigenetic age acceleration with Dasatinib and Quercetin treatment, but not with Fisetin addition.
A recent study published in Nature Aging suggests that mechanical damage to the cell membrane can induce cellular senescence, a state characterized by cell cycle arrest and tissue dysfunction. This mechanism involves calcium ion influx and the tumor suppressor gene p53, offering new insights into the aging process.
Researchers found that impaired mitochondrial unfolded protein response causes accelerated telomere shortening in both oocytes and somatic cells of aging mice. This study highlights the link between loss of mitochondrial protein homeostasis, infertility, and somatic aging.
Researchers identified senescence-related tumor microenvironment genes associated with poor prognosis, genetic alterations, and reduced responsiveness to immunotherapy in HNSC. The study highlights the importance of precision medicine approaches for personalized treatment.
Senescent tumour cells generated by chemotherapy can create an environment that helps tumour cells escape treatment. Eliminating these cells with immunotherapy boosts the effectiveness of chemotherapy.
Researchers at UC Riverside have identified a crucial protein that controls plant responses to stress and aging. The discovery reveals the importance of Golgi bodies in maintaining cellular health and highlights their potential role in human aging.
A study published in PNAS reveals that HKDC1 protein plays a crucial role in maintaining mitochondrial and lysosomal function, thereby preventing cellular senescence. The researchers found that HKDC1 helps regulate the removal of damaged mitochondria through mitophagy and facilitates lysosomal repair.
Researchers identified Benidipine as a compound promoting the death of cigarette smoke-induced senescent lung cells, improving lung emphysema. The dihydropyridine family of calcium channel blockers constitutes a new class of senolytics that could improve lung diseases.
The study found that solely the omicron variant influences cell cycle genes, leading to increased p21 expression and a senescence-associated secretory phenotype. This results in premature cellular senescence, potentially contributing to the reported cytokine storm and development of long-COVID.
A study published in EMBO Reports reveals that microautophagy is crucial for repairing damaged lysosomes, which helps prevent cellular aging. The researchers identified key regulators of this process, including STK38 and GABARAPs, and found that their depletion increases the rate of senescent cells and shortens lifespan in C. elegans.
Cancer cells' uncontrolled growth leads to a loss of ability to divide due to genetic damage accumulation. Simultaneous treatment with growth and division inhibitors can restore cellular function.
Mitochondria's dual evolutionary origin means their DNA accumulates damage as we age, contributing to age-related decline. Researchers found that defective mitochondria are removed through a unique biological process involving enzymes normally used for cell death.