Articles tagged with Cellular Senescence
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.
Researchers found that metformin + leucine (MET+LEU) treatment prevents myotube atrophy by reversing cellular senescence and improving proteostasis. The study used C2C12 myoblasts, aged mouse single myofibers, and human primary myotubes to demonstrate MET+LEU's skeletal muscle cell-autonomous properties.
Research by Whitehead et al. reveals that cellular senescence triggers amyloidosis through changes in small extracellular vesicles and extracellular matrix composition. The study provides novel insights into the formation of aortic medial amyloid and offers potential therapeutic targets for mitigating its effects.
Researchers explore cellular senescence's complex relationship with growth stimulation and cell cycle arrest, revealing potential anti-aging drug targets. Understanding these mechanisms is crucial for developing new treatments for age-related diseases.
Glioblastoma patients have a median survival time of 15 months due to the rapid infiltration of brain tissue. Cellular senescence, previously thought to be only a marker of aging, is now linked to cancer progression, with senescent cells promoting tumor growth and immune evasion.
Researchers found that clearance of p16Ink4a-positive cells did not impact β-cell mass, but improved β-cell function and proliferative capacity in a subset of HFD mice. The targeted subpopulation of β-cells is non-proliferative and non-SASP producing.
Researchers from the Salk Institute have found that deteriorating neurons from people with Alzheimer's disease undergo a late-life stress process called senescence, leading to brain inflammation and neurodegeneration. By targeting these senescent cells with therapeutics, scientists hope to prevent or treat Alzheimer's disease.
Researchers found that combining BCL-2 inhibitors can selectively eliminate senescent cells, improving efficacy and reducing toxicity by targeting high-MCL-1 expressing subpopulation of cells. This synergistic approach enables lower doses of drugs to be used, overcoming resistance to monotherapy.
A new study published in Frontiers found that excessive blue light exposure can alter cellular functions in fruit flies, potentially leading to accelerated aging. The researchers discovered changes in metabolites essential for cell function and communication between neurons.
Peter Adams and Bing Ren will map senescent cells in five tissues using state-of-the-art technologies to analyze gene expression and chromatin structures. The project seeks to reveal how and where aging cells accumulate, ultimately generating an atlas that can help develop strategies to prevent and treat age-related diseases.
Researchers discovered that liver cancer cells modify their metabolism to leave them susceptible to disruptions in arginine supply, a key molecule. A three-pronged approach targeting tumor metabolism, blocking survival-promoting responses, and starving tumors of arginine can induce senescence, making cancer cells killable.
Researchers at The Wistar Institute discovered that the enzyme ADAR1 plays a crucial role in regulating cellular senescence and tissue aging through a mechanism independent of RNA editing. This finding may lead to new therapeutic strategies for age-related disorders, such as cancer, neurodegeneration, and cardiovascular disease.
A new study reveals that oxidative damage to telomeres can trigger cellular senescence, leading to the development of 'zombie cells'. Researchers found that damage at telomeres disrupts DNA replication and induces stress signaling pathways, contributing to age-related diseases.
Researchers identified DNA damage-inducible transcript 4 (DDIT4) as a critical factor regulated by histone deacetylase 4 (HDAC4) in skin aging. Overexpression of HDAC4 rescued cells from senescence, while DDIT4 overexpression reversed changes associated with aging.
Researchers from Osaka University discovered that MondoA protein delays cellular senescence by activating autophagy, promoting longevity. Activation of MondoA also maintains mitochondrial stability, preventing senescence in tissues like the kidney.
Researchers at the Buck Institute discovered a naturally occurring metabolite, 25-hydroxycholesteral, that significantly reduces senescent cells in multiple cell types and improves muscle mass in aged mice. The molecule targets CRYAB, a small heat shock protein associated with age-related diseases like myopathies.
A study reveals how CSDE1 coordinates skin cell senescence, slowing down cellular function without causing death. This leads to the formation of a firewall against cancer, suppressing tumor growth.
Researchers at Kobe University discover that adding Vitamin B2 to stressed cells increases mitochondrial energy production and prevents cellular senescence. This finding has potential implications for preventing age-related disorders and extending healthy lifespans.
A study in mice found that senescent cells can lead to chronic stress and tissue damage, causing kidney problems. Eliminating these cells can reverse some premature tissue damage and potentially alleviate cardiovascular disease.
A research team at the University of Montreal Hospital Research Centre has found that cellular aging is caused by irreversible damage to the genome, not just telomere erosion. This discovery challenges the long-held scientific model and opens up new research opportunities for preventing cellular aging and genomic instability.
The NIH has awarded $7.5 million to Washington University School of Medicine to study senescent cells, which are thought to contribute to aging and disease. Researchers will map the location and function of senescent cells in bone marrow and liver tissues.
Researchers at Yale Cancer Center are launching a new tissue mapping center to study the role of senescent immune cells in development, aging, and disease. The goal is to develop strategies to target senescent cells to battle aging and cancer.
Researchers at Buck Institute will identify and characterize senescent cells in human ovaries, breast tissue, and skeletal muscle to better understand their role in age-related diseases. The study aims to develop therapeutics to improve human health by quelling the damaging effects of senescent cells.
Researchers create maps of senescence in heart and lung cells, comparing different types of senescent cells across the lifespan. The goal is to understand how senescent cells contribute to age-related diseases and develop therapies called senolytics.
Recent studies suggest that aging is a malleable process influenced by physiological, genetic, dietary, and pharmaceutical interventions. The relationship between cellular senescence and immunosenescence has been largely explored, with the goal of developing improved therapeutics to conserve vitality as we age.
The Buck Institute has been awarded a $14.3 million grant from the NIH to study cellular senescence, a hallmark of aging, as a driver of Alzheimer's disease and other age-related dementias. Researchers will investigate new mechanisms that can be developed into interventions to treat patients.
Researchers at Université de Montréal and McGill University have discovered a new multi-enzyme complex that reprograms metabolism and overcomes cellular senescence. The enzyme complex, named HTC, can inhibit cells from aging and has potential applications in treating various cancers.
A recent study published in Cell Metabolism found that reducing naturally occurring errors in protein synthesis improves both health and lifespan. By engineering a mutation in ribosomes, researchers observed fewer protein mistakes and improved heat resistance, leading to longer lifespans in yeast, worms, and fruit flies.
A KAIST research team used simulations to identify an enzyme that can reverse cellular senescence, a natural process contributing to aging and age-related diseases. By targeting the enzyme PDK1, cells were able to re-enter the cell cycle without proliferating abnormally.
The study identifies four distinct states of cellular senescence, each characterized by changes in metabolic and epigenomic processes. These states are linked to different levels of inflammation and metabolism, offering new insights into the aging process and potential ways to promote healthy longevity.
Researchers at Kumamoto University discovered that NSD2 enzyme prevents cellular senescence by maintaining cell growth and serum response. Reduced NSD2 leads to increased expression of genes related to cell aging and decreased activity of growth-promoting genes.
Astrocyte senescence is linked to excitotoxicity in cortical neurons involved in memory, highlighting aging as a major risk factor for neurodegeneration. The study identifies targets for drug development to slow pathology.
Aging retinal pigment epithelial cells undergo senescence due to increased oxidative stress, leading to age-related macular degeneration. Researchers found that inhibiting post-translational modifications, specifically SUMOylation, can alleviate this process, reducing SASP genes expression and proinflammatory factors.