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Dexmedetomidine Stimulates Cellular Senescence of Lung Cancer Cells Via NOX5.

Dexmedetomidine is a highly selective α- 2 adrenergic receptor agonist which has been considered as a promising anticancer agent. However, t … associated-β- galactosidase (SA-β-Gal) staining assay demonstrates that Dexmedetomidine stimulated cellular senescence by activating the p53/p16 signaling. Additionally, treatment with Dexmedetomidine led to increased ROS production and the expression of γH2AX, implicating typical DNA damage in lung cancer cells. Interestingly, Dexmedetomidine increased the expressi …

Circadian Gene BMAL1 Regulation of Cellular Senescence in Thyroid Aging.

As global aging accelerates, the incidence of thyroid diseases, particularly hypothyroidism, is rising in the elderly. The thyroid-stimulating hormone (TSH) levels increase in healthy elderly populations. However, whether the thyroid undergoes cellular senescence and how this relates to thyroid hormone (TH) synthesis remain unclear. To investigate the molecular and functional characteristics of thyroid aging, we performed scRNA-seq on human thyroids from young, middle-aged, and old groups, identifying thousands of aging-related differentially expressed genes and revealing the early onset of ag…

The drug discovery and therapeutic nano-strategies targeting cellular senescence.

Cellular senescence is a primary driver of aging, where damaged or senescent cells (SnCs) continuously accumulate in the body, altering the local tissue environment and causing various pathologies in different organs or tissues, offering brand-new diagnostic and therapeutic possibilities for aging-related disease. This review begins by discussing the multiple molecular mechanisms of cellular senescence. We mainly focus on the therapeutic strategies and their clinical applications targeting cellular senescence, where senolytic and senomorphic drugs are currently two main categories of anti-agin…

Ускоренная клеточная сенсация в прогрессивном многоразовом склерозе: гистопатологическое исследование.

ЦЕЛЬ: Неверодегенеративные процессы, приводящие к росту инвалидности при прогрессивном множественном склерозе (P-MS), не были в полной мере разъяснены. Последние данные увязывают клеточную сенсацию (CS) с нейродегенерацией. Мы расследовали доказательства CS в P-MS и пытались определить их структуру. Мы использовали 53BP1, p16 и липофускин в качестве маркеров CS при повреждениях белого материала (WML), обычном виде белого вещества (NAWM), обычном виде кортикального серого вещества (NAGM), контроле белого вещества (CWM) и контроле серого вещества (CGM) при вскрытии материала пациента с P-MS и зд

Совпадение в аннотации оригинала
OBJECTIVE: The neurodegenerative processes driving the build-up of disability in progressive multiple sclerosis (P-MS) have not been fully elucidated. Recent data link cellular senescence (CS) to neurodegeneration. We investigated for evidence of CS in P-MS and sought to determine its pattern. METHODS: We used 53BP1, p16, and lipofuscin as markers of CS in …

Prx1/PHB2 axis mediates mitophagy in oral leukoplakia cellular senescence.

BACKGROUND: Oral leukoplakia (OLK) is the most common oral potentially malignant disorder (OPMD), which can be malignantly transformed into oral squamous cell carcinoma (OSCC). Peroxiredoxin1(Prx1) has been predicted to bind to Prohibitin2 (PHB2), which confers to affect OLK progression; however, the mechanism of Prx1/PHB2 mediated mitophagy involved in OLK remains unclear. METHODS: This study aimed to explore the mechanism of the Prx1/PHB2 axis on senescence in OLK through mediating mitophagy. The positive rate of Ki67 and the expression of p21, p16, PHB2, and LC3 in human normal, OLK, and O

Mapping epidermal and dermal cellular senescence in human skin aging.

Single-cell RNA sequencing and spatial transcriptomics enable unprecedented insight into cellular and molecular pathways implicated in human … ns of senescent cells, a sign of biological aging, compared to chronological aging. A skin-specific cellular senescence gene set, termed SenSkin™, was curated and confirmed to be elevated in the context of photoaging, chronological aging, and non-replicating CDKN1A+ (p21) cells. In the epidermis, senescent melanocytes were associated with elevated melanin synthesis, …

Therapeutic approaches targeting aging and cellular senescence in Huntington's disease.

Huntington's disease (HD) is a devastating neurodegenerative disease that is manifested by a gradual loss of physical, cognitive, and mental abilities. As the disease advances, age has a major impact on the pathogenic signature of mutant huntingtin (mHTT) protein aggregation. This review aims to explore the intricate relationship between aging, mHTT toxicity, and cellular senescence in HD. Scientific data on the interplay between aging, mHTT, and cellular senescence in HD were collected from several academic databases, including PubMed, Google Scholar, Google, and ScienceDirect. The search ter…

Cellular Senescence in Craniofacial Tissue Regeneration: Inducers, Biomarkers, and Interventions.

Craniofacial defects and dental tissue loss have significant negative impacts on the structure and function of jaws and face, often resulting in psychological issues in patients, emphasizing the urgent need for effective craniofacial tissue reconstruction. Unfortunately, natural regeneration of these tissues is limited. Dental-derived mesenchymal stem cells (MSCs) have emerged as a promising resource for tissue engineering-based therapeutic approaches. However, the clinical outcomes of MSC-based transplantation have not met expectations due to various complex reasons, and cellular senescence i…

Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury.

Traumatic brain injury (TBI) is associated with mortality and morbidity worldwide. Accumulating pre-clinical and clinical data suggests TBI … chronic, low-grade sterile inflammation associated with natural aging, promotes cognitive decline. Cellular senescence and the subsequent development of a senescence associated secretory phenotype (SASP) promotes inflammaging and cognitive aging, although the functional association between senescent cells and neurodegeneration is poorly defined after TBI. In this mi …

Nicotinamide Improves Skin Photoaging in Mice by Delaying Cellular Senescence and Suppressing the Senescence-Associated Secretory Phenotype.

Nicotinamide (NAM), a precursor of nicotinamide adenine dinucleotide (NAD+), and NAD+ are integral to a variety of cellular processes. NAM supplementation has been shown to have benefits for cellular senescence. However, the mechanism by which NAM improves skin photoaging remains unclear. In this study, the multi-omics analysis revealed that insufficient nicotinamide metabolism may be associated with a decrease in NAD+ synthesis during skin aging. Importantly, we found that NAM has an ameliorating effect on the skin photoaging in mice. Supplementation with NAM restored the expression of the sa…

Targeted apoptosis of senescent cells by valproic acid alleviates therapy-induced cellular senescence and lung aging.

BACKGROUND: Accumulation of senescent cells in tissues and their downstream effect programs have emerged as key drivers of aging and age-ass … tions from approved drugs. METHODS: The effects of valproic acid (VPA), a derivative of valine, in cellular senescence were evaluated by senescence-associated β galactosidase (SA-β-Gal) staining, flow cytometry and western blot (WB). The cell viability was tested using CCK-8 kits. Cell apoptosis was detected by Annexin V-EGFP/PI apoptosis detection kit. Cell autopha …

Effects and Therapeutic Strategies of Intra-Hepatic Cellular Senescence and Regeneration.

The liver constitutes a vital organ characterized by remarkable regenerative capacity, wherein intra-hepatic cellular senescence and regeneration exert pivotal regulatory functions in maintaining hepatic homeostasis and in developing therapeutic interventions for liver diseases. Intra-hepatic cellular aging is typically characterized by diminished proliferative capacity, genomic instability, mitochondrial dysfunction, and exacerbated inflammatory responses, all of which contribute to hepatic functional impairment and the pathogenesis of associated diseases. Liver regeneration depends upon the …

Effects of micro- and nano-plastics exposure on cellular senescence: an overview.

Micro- and nano-plastics (MNPs) contamination has recently become a widespread concern. These particles have been detected in multiple human organs. MNPs can enter the human body through three ways: diet intake, inhalation and skin contact, subsequently entering the bloodstream and distributing throughout the body's tissue systems. The health risks posed by MNPs exposure are believed to be linked to cellular senescence, a state of stable cell growth arrest that significantly increases the risk of age-related diseases. The mechanisms of MNPs-induced cellular senescence are primarily associated …

Cellular Senescence and SASP in Bladder Ageing: Mechanisms and Emerging Interventions.

Bladder dysfunction is a prevalent age-related condition that severely impairs quality of life in older adults and commonly manifests as lower urinary tract symptoms (LUTS), including frequency, urgency, incontinence, and nocturia. Cellular senescence, characterized by irreversible cell-cycle arrest accompanied by persistent metabolic activity, is increasingly recognized as a contributor to age-associated tissue degeneration. Senescent cells secrete a diverse array of inflammatory cytokines, chemokines, growth factors, and matrix-remodeling enzymes, collectively termed the senescence-associate…

Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder in the elderly, characterized by extracellular amyloid β‑ (Aβ) plaque deposition and intracellular neurofibrillary tangles (NFTs). Impaired autophagy, the cellular pathway for degrading damaged organelles and misfolded proteins, and cellular senescence, permanent cell cycle arrest with proinflammatory secretions, have emerged as key contributors to AD pathogenesis. METHODS: We performed a narrative review of recent mechanistic and preclinical studies investigating (1) autophagic flux and its role in Aβ and tau cl…

Targeting Cellular Senescence for Healthy Aging: Advances in Senolytics and Senomorphics.

BACKGROUND: Cellular senescence is a fundamental characteristic of aging, marked by permanent cell cycle cessation and the release of pro-inflammatory mediators. Although senescence plays advantageous roles in tissue regeneration and tumor suppression, its accumulation leads to aging-related illnesses and functional deterioration. OBJECTIVE: This review examines the processes of cellular senescence, its effects on aging and age-related disorders, and emerging therapeutic strategies to modulate senescence for promoting healthy aging. METHODS: A thorough literature review was performed using p…

Cellular senescence: A novel mechanism of therapeutic resistance in prostate cancer.

Prostate cancer (PCa) is a leading cause of cancer-related morbidity and mortality. Despite the efficacy of androgen deprivation therapy (ADT), patients with advanced PCa eventually progress to a lethal castration-resistant disease state. Cellular senescence represents a stable growth arrest induced by stress signaling cascades or cancer therapeutics, and escape from a senescent state may be implicated in the development of castration resistance. We discuss the mechanisms promoting cellular senescence in PCa and its contribution to therapeutic resistance to ADT, PARP inhibitors, chemotherapy, …

Role of Cellular Senescence in IUGR: Impact on Fetal Morbidity and Development.

Intrauterine growth restriction (IUGR) is a critical challenge in perinatal medicine and is associated with significant morbidity and mortality. This review explores the intricate involvement of early developmental senescence in IUGR. We highlight the dual role of cellular senescence in both normal development and pathological conditions, emphasizing the need for further research to elucidate these mechanisms and develop targeted interventions. We discuss how oxidative stress and mitochondrial dysfunction affect senescence determinants. We present emerging therapeutic strategies aimed at targe…

The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.

Cellular senescence is a stress responsive program that critically affects chronological and biological aging, ischemia reperfusion injury (IRI), and age related cardiovascular diseases. Of relevance, cardiac senescent cells exhibit altered characteristics that promote inflammation, remodeling, and fibrosis, ultimately contributing to the functional decline following myocardial infarction (MI). At the same time, emerging evidence suggests that senescence may also exert protective effects post-MI, limiting fibrosis. Thus, understanding the mechanisms and pathways of cardiac senescence appears c…