Articles tagged with 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.
A new study has revealed a molecular fingerprint of biological aging, shedding light on why people age differently. The researchers identified 25 metabolites that can reflect biological age, known as the Healthy Aging Metabolic (HAM) Index, which was found to be more accurate than other aging metrics.
Researchers define a 'core senescent profile' in human colon fibroblasts, revealing potential driver proteins involved in CRC. The study's findings provide insights into therapies for improving overall health and preventing CRC.
A new probe has been developed to detect senescent cells in organs, which are associated with many age-related diseases. The probe interacts with an enzyme abundant in senescent cells, producing a fluorescent compound excreted in the urine.
Researchers at Mayo Clinic shed light on the biology of zombie cells and their link to aging-related health issues. A study found that specific senescent biomarkers can predict mortality beyond chronological age and chronic disease presence.
Researchers at Memorial Sloan Kettering Cancer Center have engineered CAR T cells to target senescent cells, which can lead to chronic inflammation with aging. The treatment improved metabolic function in older mice and prevented decline later in life, suggesting potential benefits for diseases associated with 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.
Researchers found that ovarian cancer cells spread more easily in tissues that are senescent or aged due to the secretion of a unique extracellular matrix. This matrix attracts cancer cells and allows them to attach and spread faster, potentially leading to worse outcomes in older populations.
A groundbreaking study found that combining partial normoxic recovery with senolytic Navitoclax significantly reduced sleepiness and improved cognitive function in mice with OSA. This suggests targeting accelerated senescence may be a promising avenue for improving treatment outcomes.
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.
This study found that SIRT6 activation improves DNA damage repair efficiency and reduces baseline DNA damage in chondrocytes from older donors. MDL-800 treatment also lowered p16 promoter activity and decreased DNA damage in murine cartilage explants, supporting the concept of SIRT6 as a critical regulator of DNA repair.
A new study found that HSP10 treatment improved exploratory preferences, object contacts, and swimming time in aged mice, while also increasing proliferating cells and differentiated neuroblasts. The protein also mitigated age-related gene reductions and increased sirtuin 3 levels.
Researchers found that aging can accelerate evolution, favoring faster adaptation to changing worlds. This means senescence becomes an advantageous characteristic under natural selection.
Transplanting older organs from donors accelerates aging in younger recipients, leading to impaired physical capacity and cognitive decline. Senolytic treatments have shown promise in reducing these effects by inhibiting senescence-associated factors.
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.
Researchers at Hokkaido University found that cancer stem cells cause macrophages to age, suppressing their antitumor activity. Supplementing mice with nicotinamide mononucleotide restored macrophage function and prevented tumor growth.
Researchers have identified a potential treatment for lower back pain by targeting senescent osteoclasts in the vertebral column of mice. Using anti-senescent drugs like Navitoclax may relieve spinal sensitivity and reduce pain, according to the study published in eLife.
Researchers found that higher alcohol consumption is associated with biological age acceleration and hypertension in middle-aged and older adults, but not in young adults. The study suggests that alcohol consumption may mediate the association between alcohol intake and quantitative traits like hypertension.
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 found that DNA damage accumulates in arteries with aging and contributes to impaired vascular function. In mice lacking or heterozygous for the double-strand DNA break repair protein ATM kinase, aging accelerated vascular dysfunction, including increased arterial stiffness and oxidative stress.
A research team has developed a technology that selectively targets and eliminates aging cells, contributing to various inflammatory conditions. This approach represents a new paradigm for treating age-related diseases with minimal toxicity concerns.
Researchers at Mayo Clinic discovered that senescent macrophages in the lung promote tumor growth by blocking the immune system's response to abnormal cell growth. Eliminating these senescent cells delays tumor formation, suggesting a potential therapeutic target for cancer treatment.
Microglial cells age differently in male and female mice, with female microglia displaying a 'middle-aged' phenotype and male microglia switching suddenly to an aged phenotype. The researchers identified key genes and mechanisms contributing to this aging process, including the role of aged-like microglia in cognitive decline.
Researchers found that a healthy diet from an early age can suppress senescence and loss of fitness in yeast, even late in life. The study proposes an alternative to calorie restriction for improving healthy ageing through dietary change.
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.
Researchers investigated hepatic hydrogen sulfide production in a mouse model of Hutchinson-Gilford Progeria Syndrome (HGPS) and found reduced H2S levels in RC-fed mice, with partial rescue on high-fat diet. This study suggests that accelerated aging in HGPS may be partially explained by reduced hepatic H2S levels.
A recent study suggests that Black Americans experience accelerated biological aging compared to White Americans, primarily due to lower socioeconomic status and exposure to air pollution. The findings highlight the significant impact of environmental factors on epigenetic aging disparities between racial groups.
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 new drug delivery method utilizes polymer-stabilized crystals to deliver antioxidants to stem cells, minimizing variation in drug release and extending the duration of effectiveness. This technology can be applied to various cell cultures and potentially other hydrophilic drugs, disease models, and methods applications.
Cancer cells can hide and escape therapies leading to recurrence. Researchers identify three possible mechanisms: cancer stem cells, polyploidy, and senescence. Combination treatments involving chemoradiation-induced transitory senescence and senolytic therapies may be effective in preventing repopulation.
Researchers have developed a test to detect 'zombie' cells in donor blood, which may help increase the number of suitable hearts available for transplant. The test targets proteins associated with senescent cells, which can impact heart health.
Scientists at Medical College of Georgia are investigating the impact of HIV treatment on bone and muscle aging. They found that common antiretroviral cocktails can accelerate aging by about a decade, leading to increased inflammation and oxidative stress in bone marrow stem cells.
Researchers discover a molecule that destroys aged cells without affecting healthy ones, paving the way for delaying tissue ageing. Testing with animal models will now begin to explore its potential anti-cancer effects and improve life expectancy.
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.
Researchers have identified distinct senescence subpopulations and dynamic changes in the transcriptome of human cells undergoing senescence. The study provides new understanding of the heterogeneous nature of senescence and its impact on aging diseases.
Researchers from Integrated Biosciences developed an AI platform to discover novel senolytic compounds, a class of molecules targeting age-related processes. The platform identified three highly selective and potent compounds with favorable medicinal chemistry properties.
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.
A large-scale study has linked accelerated biological aging to an increased risk of depression and anxiety in older adults. Adults with more advanced biological age were found to be more likely to develop depression and anxiety over time compared to peers who were biologically younger.
A study found that biological age in humans and mice increases rapidly in response to diverse forms of stress, only to reverse after recovery. The researchers used DNA methylation clocks to measure changes in biological age, revealing transient changes in response to stressful stimuli.
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.
Researchers found that senescent cells promote regeneration by secreting factors that stimulate nearby muscle tissue to produce new muscle cells. The presence of these cells enhances the regeneration process, allowing salamanders to grow lost limbs in a matter of weeks.
Researchers at the University of Minnesota Medical School found that genetic background and social rank are critical contextual modifiers of aging and lifespan in animal models. They discovered that low social status corresponds to a shorter lifespan, but with varying effects depending on the individual's genetic predisposition.
A study found that regular exercise increases mitochondrial fusion, benefiting muscle cells and maintaining physical fitness even in old age. Daily sessions of exercise throughout life delay the accumulation of dysfunctional mitochondria and decline in physical fitness.
Researchers found that senescence-associated exosomes (SA-EXOs) from MSCs induce fibrosis and activate invasive characteristics in neighboring cells via the TGF-β pathway. SA-EXOs play a large role in cancer-related fibrosis, and their unique miRNA content influences myofibroblast phenotypes.
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.
Researchers examined three epigenetic age acceleration measurements and found inverse associations with lung cancer risk in men and younger participants. However, these findings did not support a positive association between epigenetic age measures and lung cancer risk in the study.
Researchers identified 17 clusters of single cells in peripheral blood, showing upregulation of antigen processing and presentation pathways and downregulation of genes involved in ribosome pathways with age. The study also found senescent T cells resistant to apoptosis, potentially targeted for treatment.
A new study finds epigenetic aging is associated with aberrant neural oscillatory dynamics serving visuospatial processing in people with HIV. Participants showed accelerated biological age and different brain activity patterns compared to controls, suggesting a link between biological aging and neural function in PWH.
Adults with higher serum sodium levels were more likely to develop chronic conditions, show signs of advanced biological aging, and die at a younger age. Optimal hydration may be associated with slower aging and reduced risk of chronic diseases.
A 16-year longitudinal study found associations between DNA methylation-based measures and neuropsychologically-validated cognitive decline in midlife. The results suggest that these measures may serve as biomarkers for a molecular aging mechanism, potentially identifying individuals at risk of cognitive impairment and dementia.
Researchers discovered that damaged cells and aging induce high levels of oxidative stress and DNA damage in a subset of cells, leading to senescence. Senescent cells repress muscle regeneration by releasing inflammatory factors, while also promoting fibrosis, highlighting the need to remove these cells for improved repair.
A team of researchers identified senescent cells as a major obstacle to muscle regeneration, which can be overcome genetically or pharmacologically. Neutralizing these cells improves tissue repair in both young and elderly individuals.
A study published in Aging-US reveals changes in gene expression associated with age-related muscle loss and frailty. Researchers identified unique cellular subpopulations in aged and sarcopenic skeletal muscle, which may facilitate the development of new treatments for age-related frailty.
A new study found that obeticholic acid can reverse cognitive impairment in patients with cholestatic liver disease, improving short-term memory and restoring brain function. The study used a rodent model of bile duct ligation-induced cholestasis and found that the drug significantly improved cognitive deficits.
Johannes Gutenberg University Mainz has been awarded funding for three Collaborative Research Centers in the life sciences, including CRC 1551 and CRC/Transregio 355. The centers will focus on investigating polymer concepts in cellular function and heterogeneity of regulatory T cells in distinct microenvironments.
The German Research Foundation renewed CRC 1361 for an additional four years to explore mechanisms of DNA repair and genome stability. The consortium aims to elucidate how cells safeguard genetic information and promote human health by understanding DNA damage signaling pathways.
Researchers found that glutaminase inhibitor BPTES selectively eliminates senescent dermal fibroblasts, improving skin aging phenotype by increasing collagen density and cell proliferation. The study suggests BPTES as a potential therapeutic agent for skin aging, offering new treatment options.