Cellular senescence in brain aging and cognitive decline DOI Creative Commons
Areez Shafqat, Saifullah Khan, Mohamed H. Omer

et al.

Frontiers in Aging Neuroscience, Journal Year: 2023, Volume and Issue: 15

Published: Nov. 23, 2023

Cellular senescence is a biological aging hallmark that plays key role in the development of neurodegenerative diseases. Clinical trials are currently underway to evaluate effectiveness senotherapies for these However, impact on brain and cognitive decline absence neurodegeneration remains uncertain. Moreover, patient populations like cancer survivors, traumatic injury obese individuals, obstructive sleep apnea patients, chronic kidney disease patients can suffer age-related changes prematurely, suggesting they may accelerated brain. Understanding neurocognitive deficits linked conditions crucial, especially considering rapidly evolving field senotherapeutics. Such treatments could help alleviate early significantly reducing morbidity healthcare costs. This review provides translational perspective how cellular decline. We also discuss important caveats surrounding mainstream senolytics senomorphics, present emerging evidence hyperbaric oxygen therapy immune-directed therapies as viable modalities senescent cell burden.

Language: Английский

Pathological mechanisms of kidney disease in ageing DOI
Takeshi Yamamoto, Yoshitaka Isaka

Nature Reviews Nephrology, Journal Year: 2024, Volume and Issue: 20(9), P. 603 - 615

Published: July 18, 2024

Language: Английский

Citations

18

Breast cancer: pathogenesis and treatments DOI Creative Commons
Xin Xiong,

Lewei Zheng,

Yu‐Qiang Ding

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2025, Volume and Issue: 10(1)

Published: Feb. 18, 2025

Abstract Breast cancer, characterized by unique epidemiological patterns and significant heterogeneity, remains one of the leading causes malignancy-related deaths in women. The increasingly nuanced molecular subtypes breast cancer have enhanced comprehension precision treatment this disease. mechanisms tumorigenesis progression been central to scientific research, with investigations spanning various perspectives such as tumor stemness, intra-tumoral microbiota, circadian rhythms. Technological advancements, particularly those integrated artificial intelligence, significantly improved accuracy detection diagnosis. emergence novel therapeutic concepts drugs represents a paradigm shift towards personalized medicine. Evidence suggests that optimal diagnosis models tailored individual patient risk expected are crucial, supporting era oncology for cancer. Despite rapid advancements increasing emphasis on clinical comprehensive update summary panoramic knowledge related disease needed. In review, we provide thorough overview global status including its epidemiology, factors, pathophysiology, subtyping. Additionally, elaborate latest research into contributing progression, emerging strategies, long-term management. This review offers valuable insights Cancer Research, thereby facilitating future progress both basic application.

Language: Английский

Citations

17

Exosomal miR-302b rejuvenates aging mice by reversing the proliferative arrest of senescent cells DOI Creative Commons
Youkun Bi, Xinlong Qiao, Zhaokui Cai

et al.

Cell Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

7

Impact of glycolysis enzymes and metabolites in regulating DNA damage repair in tumorigenesis and therapy DOI Creative Commons

Fengyao Sun,

Wen Li,

Ruihang Du

et al.

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: Jan. 23, 2025

Initially, it was believed that glycolysis and DNA damage repair (DDR) were two distinct biological processes independently regulate tumor progression. The former metabolic reprogramming rapidly generates energy generous intermediate metabolites, supporting the synthetic metabolism proliferation of cells. While DDR plays a pivotal role in preserving genomic stability, thus resisting cellular senescence cell death under both physiological radio-chemotherapy conditions. Recently, an increasing number studies have shown closely correlation between these processes, then promoting For instance, lactic acid, product glycolysis, maintains acidic microenvironment not only fosters invasion but also facilitates by enhancing AKT activity. Here, we provide comprehensive overview enzymes metabolites involved along with primary methods for DDR. Meanwhile, this review explores existing knowledge regulating Moreover, considering significant roles development resistance, present discusses effective direct or indirect therapeutic strategies targeted to

Language: Английский

Citations

4

The intersection of aging and estrogen in osteoarthritis DOI Creative Commons
Aysegul Atasoy‐Zeybek,

Kelly K. Showel,

Christopher V. Nagelli

et al.

npj Women s Health, Journal Year: 2025, Volume and Issue: 3(1)

Published: Feb. 25, 2025

Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degradation, inflammation, and pain. While multiple factors contribute to OA development, age sex are primary risk factors, particularly affecting postmenopausal women. The dramatic increase in after menopause suggests estrogen deficiency accelerates progression. This review explores the molecular mechanisms connecting aging focusing on key genes pathways identified through RNA sequencing.

Language: Английский

Citations

2

Immunosenescence promotes cancer development: from mechanisms to treatment strategies DOI Creative Commons

Leihan Wang,

Tang Dong

Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 10, 2025

The body's innate immune system plays a pivotal role in identifying and eliminating cancer cells. However, as the ages, its functionality can deteriorate, becoming dysfunctional, inefficient, or even inactive—a condition referred to immunosenescence. This decline significantly increases risk of malignancies. While pro-cancer effects T-cell aging have been widely explored, there remains notable gap literature regarding impact on cells, such macrophages neutrophils. review seeks address this gap, with emphasis these cell types. Furthermore, although certain immunotherapies, including checkpoint inhibitors (ICIs), demonstrated efficacy across broad spectrum cancers, elderly patients are less likely derive clinical benefit from treatments. In some cases, they may experience immune-related adverse events (irAEs). senolytic strategies shown promise exerting anti-cancer effects, their reactions potential off-target present significant challenges. aims elucidate immunosenescence, implications for safety ICIs, anti-aging treatment strategies. addition, optimizing therapies minimize enhance therapeutic outcomes critical focus future research endeavors. Senescence is an inevitable phenomenon human body, scientists explored specific mechanisms by which immunosenescence advances development cancer. summarizes characteristics be used level surveillance cancers due "Targeting immunosenescence" new idea strategy therapy.

Language: Английский

Citations

2

Neutrophils in aging and aging‐related pathologies DOI Creative Commons

Kristof Van Avondt,

Jan‐Kolja Strecker, Claudia Tulotta

et al.

Immunological Reviews, Journal Year: 2022, Volume and Issue: 314(1), P. 357 - 375

Published: Oct. 31, 2022

Over the past millennia, life expectancy has drastically increased. While a mere 25 years during Bronze and Iron ages, in many European countries Japan is currently above 80 years. Such an increase result of improved diet, style, medical care. Yet, increased span aging also represent most important non-modifiable risk factors for several pathologies including cardiovascular disease, neurodegenerative diseases, cancer. In recent years, neutrophils have been implicated all these pathologies. Hence, this review provides overview how impacts neutrophil production function conversely drive aging-associated Finally, we provide perspective on processes neutrophil-driven context can be targeted therapeutically.

Language: Английский

Citations

63

NAD metabolism: Role in senescence regulation and aging DOI Creative Commons
Claudia C.S. Chini,

Heidi Soares Cordeiro,

Ngan Tran

et al.

Aging Cell, Journal Year: 2023, Volume and Issue: 23(1)

Published: July 9, 2023

Abstract The geroscience hypothesis proposes that addressing the biology of aging could directly prevent onset or mitigate severity multiple chronic diseases. Understanding interplay between key aspects biological hallmarks is essential in delivering promises hypothesis. Notably, nucleotide nicotinamide adenine dinucleotide (NAD) interfaces with several aging, including cellular senescence, and changes NAD metabolism have been shown to be involved process. relationship senescence appears complex. On one hand, accumulation DNA damage mitochondrial dysfunction induced by low + can promote development senescence. other state occurs during may inhibit SASP as this secretory phenotype are both highly metabolically demanding. However, date, impact on progression has not fully characterized. Therefore, explore implications replacement therapies, it consider their interactions We propose a comprehensive understanding boosting strategies senolytic agents necessary advance field.

Language: Английский

Citations

38

Hallmarks of ageing in human skeletal muscle and implications for understanding the pathophysiology of sarcopenia in women and men DOI Creative Commons
Antoneta Granic, Karen Suetterlin,

Tea Shavlakadze

et al.

Clinical Science, Journal Year: 2023, Volume and Issue: 137(22), P. 1721 - 1751

Published: Nov. 1, 2023

Abstract Ageing is a complex biological process associated with increased morbidity and mortality. Nine classic, interdependent hallmarks of ageing have been proposed involving genetic biochemical pathways that collectively influence trajectories susceptibility to pathology in humans. skeletal muscle undergoes profound morphological physiological changes loss strength, mass, function, condition known as sarcopenia. The aetiology sarcopenia whilst research this area growing rapidly, there relative paucity human studies, particularly older women. Here, we evaluate how the nine classic ageing: genomic instability, telomere attrition, epigenetic alterations, proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication contribute pathophysiology We also highlight five novel particular significance inflammation, neural extracellular matrix reduced vascular perfusion, ionic dyshomeostasis, discuss are interconnected. Their clinical relevance translational potential considered.

Language: Английский

Citations

34

Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies DOI Creative Commons
Sagar Gaikwad, Sudipta Senapati, Md. Anzarul Haque

et al.

Alzheimer s & Dementia, Journal Year: 2023, Volume and Issue: 20(1), P. 709 - 727

Published: Oct. 9, 2023

Abstract Aging, tau pathology, and chronic inflammation in the brain play crucial roles synaptic loss, neurodegeneration, cognitive decline tauopathies, including Alzheimer's disease. Senescent cells accumulate aging brain, accelerate process, promote tauopathy progression through their abnormal inflammatory secretome known as senescence‐associated secretory phenotype (SASP). Tau oligomers (TauO)—the most neurotoxic species—are to induce senescence SASP, which subsequently neuropathology, inflammation, oxidative stress, dysfunction, neuronal death, dysfunction. TauO, are associated with heterogeneity decline. However, underlying mechanisms driving disease remain largely unknown, impeding development of therapies for tauopathies. Based on clinical preclinical evidence, this review highlights critical role TauO neurodegeneration. We discuss key knowledge gaps potential strategies targeting treat Highlights Senescence, oligomeric (TauO), process contributing highlight target tauopathies while addressing gaps.

Language: Английский

Citations

33