Articles tagged with Cellular Senescence
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.
Researchers discovered BMAL1 is significantly upregulated in senescent cells and modulates the senescence program through AP-1. The study highlights a previously unappreciated role of BMAL1 in regulating cellular senescence and circadian clock components.
Researchers identified abnormal keratin expression patterns in senescent ocular surface cells, which may contribute to severe ocular surface diseases. Gene expression profiles showed substantial differences between senescent and non-senescent cells, highlighting their potential role in pathology.
Researchers developed a DNA damage-induced senescence model in osteoarthritic chondrocytes, which reliably induces cellular senescence and accumulates senescent cells in OA joint tissues. The study provides a useful model to develop therapeutic approaches targeting senescence in osteoarthritis.
Researchers discovered a unique mechanism in naked mole-rats that targets senescent cells, suppressing their accumulation and delaying aging. This 'natural senolytic' process involves serotonin metabolism and oxidative stress, potentially offering an evolutionary rationale for removing senescent cells as a therapeutic strategy.
Researchers found that human senescent fibroblasts trigger progressive lung fibrosis in immunodeficient mice by inducing paracrine senescence and pro-fibrotic activities. The study also suggests that senolytic compounds like navitoclax can ameliorate lung fibrosis induced by senescent human fibroblasts.
Integrated Biosciences announces a drug discovery platform that enables precise control of the integrated stress response, a biological pathway activated by cells in response to various pathological conditions. The new platform uses optogenetic technique to study the ISR in live cells without physical or chemical damage.
Researchers discovered that a tiny sea creature, Hydractinia, regenerates its entire body with help from aging cells, providing insights into the interconnectedness of healing and aging. The study suggests that senescence may have evolved as a regeneration mechanism in ancient animals.
A research team from HKUST identified CPEB4, an mRNA-binding protein, as a key player in maintaining mitochondrial metabolism and energy production. Restoring CPEB4 expression in aged muscle stem cells improved energy production and protected against cellular senescence.
A new study published in Aging-US has identified the p53-p16/RB-E2F-DREAM complex as a critical regulator of cellular senescence. The researchers found that this complex represses multiple target genes involved in cell cycle regulation, DNA repair, and chromatin structure, leading to the stability of the senescent arrest.
Researchers tested zoledronic acid's effects on cellular senescence using multiple approaches. The study found that zoledronic acid killed senescent cells with minimal effects on non-senescent cells and reduced circulating SASP factors, including CCL7, IL-1β, TNFRSF1A, and TGFβ1.
Researchers discover that senescence-associated secretory phenotype (SASP) can induce neuroendocrine transdifferentiation (NED) in breast cancer epithelial cells, promoting tumor progression and aging-related features. SASP's dual role in cancer involves both antitumoral and tumorigenic effects.
A new study presents a chronic wound murine model that characterizes the role of persistent senescent cell accumulation in delayed wound closure. The molecular profiles of senescent cells demonstrate the adverse influence of SASP factors, highlighting a potential root-cause-driven therapeutic strategy.
Researchers found that CUDC-907 selectively induces apoptosis in cells driven to senesce by p53 expression. The compound showed senolytic properties in different models of stress-induced senescence, depending on its inhibitory effects on HDACs and PI3K.
Researchers found that p21 knockout mice experienced reduced senescent cell presence, alleviated chronic lung inflammation, and improved fitness. Resident epithelial and endothelial cells played a significant role in mediating the p21-dependent inflammatory response.
Scientists at SENS Research Foundation have discovered a new class of broad-spectrum senolytic drugs that target the key vulnerability in destructive aging cells. These drugs are effective against both primary and secondary senescent cells, making them a promising approach for treating age-related diseases.