Chronic inflammation and the hallmarks of aging

Molecular Metabolism, Год журнала: 2023, Номер 74, С. 101755 - 101755

Опубликована: Июнь 16, 2023

Recently, the hallmarks of aging were updated to include dysbiosis, disabled macroautophagy, and chronic inflammation. In particular, low-grade inflammation during aging, without overt infection, is defined as "inflammaging," which associated with increased morbidity mortality in population. Emerging evidence suggests a bidirectional cyclical relationship between development age-related conditions, such cardiovascular diseases, neurodegeneration, cancer, frailty. How crosstalk other underlies biological mechanisms disease thus particular interest current geroscience research.

Язык: Английский

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Multimodal smart systems reprogramme macrophages and remove urate to treat gouty arthritis

Nature Nanotechnology, Год журнала: 2024, Номер 19(10), С. 1544 - 1557

Опубликована: Июль 17, 2024

Язык: Английский

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Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review)

International Journal of Molecular Medicine, Год журнала: 2024, Номер 53(5)

Опубликована: Апрель 2, 2024

Chronic neuroinflammation serves a key role in the onset and progression of neurodegenerative disorders. Mitochondria serve as central regulators neuroinflammation. In addition to providing energy cells, mitochondria also participate immunoinflammatory response disorders including Alzheimer's disease, Parkinson's multiple sclerosis epilepsy, by regulating processes such cell death inflammasome activation. Under inflammatory conditions, mitochondrial oxidative stress, epigenetics, dynamics calcium homeostasis imbalance may underlying regulatory mechanisms for these diseases. Therefore, investigating related dysfunction result therapeutic strategies against chronic neurodegeneration. The present review summarizes neuroinflammatory diseases current treatment approaches that target

Язык: Английский

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Redox regulation: mechanisms, biology and therapeutic targets in diseases

Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)

Опубликована: Март 7, 2025

Redox signaling acts as a critical mediator in the dynamic interactions between organisms and their external environment, profoundly influencing both onset progression of various diseases. Under physiological conditions, oxidative free radicals generated by mitochondrial respiratory chain, endoplasmic reticulum, NADPH oxidases can be effectively neutralized NRF2-mediated antioxidant responses. These responses elevate synthesis superoxide dismutase (SOD), catalase, well key molecules like nicotinamide adenine dinucleotide phosphate (NADPH) glutathione (GSH), thereby maintaining cellular redox homeostasis. Disruption this finely tuned equilibrium is closely linked to pathogenesis wide range Recent advances have broadened our understanding molecular mechanisms underpinning dysregulation, highlighting pivotal roles genomic instability, epigenetic modifications, protein degradation, metabolic reprogramming. findings provide foundation for exploring regulation mechanistic basis improving therapeutic strategies. While antioxidant-based therapies shown early promise conditions where stress plays primary pathological role, efficacy diseases characterized complex, multifactorial etiologies remains controversial. A deeper, context-specific signaling, particularly redox-sensitive proteins, designing targeted aimed at re-establishing balance. Emerging small molecule inhibitors that target specific cysteine residues proteins demonstrated promising preclinical outcomes, setting stage forthcoming clinical trials. In review, we summarize current intricate relationship disease also discuss how these insights leveraged optimize strategies practice.

Язык: Английский

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The role of chronic low-grade inflammation in the development of sarcopenia: Advances in molecular mechanisms

International Immunopharmacology, Год журнала: 2025, Номер 147, С. 114056 - 114056

Опубликована: Янв. 11, 2025

Язык: Английский

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Research Progress on the Anti-Aging Potential of the Active Components of Ginseng

Nutrients, Год журнала: 2023, Номер 15(15), С. 3286 - 3286

Опубликована: Июль 25, 2023

Aging is a cellular state characterized by permanent cessation of cell division and evasion apoptosis. DNA damage, metabolic dysfunction, telomere mitochondrial dysfunction are the main factors associated with senescence. increases β-galactosidase activity, enhances spreading, induces Lamin B1 loss, which further accelerate aging process. It variety diseases, such as Alzheimer’s disease, Parkinson’s, type 2 diabetes, chronic inflammation. Ginseng traditional Chinese medicine anti-aging effects. The active components ginseng, including saponins, polysaccharides, peptides, have antioxidant, anti-apoptotic, neuroprotective, age-delaying damage factor aging, mechanism through ingredients ginseng reduce delay has not been comprehensively described. This review focuses on mechanisms ginseng. Furthermore, it broadens scope ideas for research natural products aging.

Язык: Английский

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DNA Damage-Mediated Neurotoxicity in Parkinson’s Disease

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(7), С. 6313 - 6313

Опубликована: Март 28, 2023

Parkinson’s disease (PD) is the second most common neurodegenerative around world; however, its pathogenesis remains unclear so far. Recent advances have shown that DNA damage and repair deficiency play an important role in pathophysiology of PD. There growing evidence suggesting involved propagation cellular PD, leading to neuropathology under different conditions. Here, we reviewed current work on First, outlined causes Second, described potential pathways by which mediates neurotoxicity PD discussed precise mechanisms drive these processes damage. In addition, looked ahead interventions targeting repair. Finally, based status research, key problems need be addressed future research were proposed.

Язык: Английский

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Autonomic nervous system imbalance during aging contributes to impair endogenous anti-inflammaging strategies

GeroScience, Год журнала: 2023, Номер 46(1), С. 113 - 127

Опубликована: Окт. 11, 2023

Abstract Inflammaging refers to the age-related low grade, sterile, chronic, systemic, and long-lasting subclinical, proinflammatory status, currently recognized as main risk factor for development progression of most common diseases (ARDs). Extensive investigations were focused on a plethora stimuli that can fuel inflammaging, underestimating partly neglecting important endogenous anti-inflammaging mechanisms could play crucial role in such state. Studies autonomic nervous system (ANS) functions during aging highlighted an imbalance toward overactive sympathetic (SNS) tone, promoting conditions, diminished parasympathetic (PNS) activity, playing anti-inflammatory effects mediated by so called cholinergic pathway (CAP). At molecular level, CAP is characterized signals communicated via vagus nerve (with possible involvement splenic nerves) through acetylcholine release downregulate inflammatory actions macrophages, key players inflammaging. Notably, decreased vagal function increased burden activated/senescent macrophages (macrophaging) probably precede several factors diseases, while reduced macrophaging be associated with relevant reduction profiles. Hypothalamic–pituitary–adrenal axis (HPA axis) another related ANS some response mainly cortisol levels. In this perspective review, we HPA, representing broadly “anti-inflammaging” mechanisms, have efficacy lose effectiveness aged people, phenomenon contribute framework, strategies aimed re-balance PNS/SNS activities explored modulate systemic inflammaging especially at early subclinical stage, thus increasing chances reach extreme limit human lifespan healthy status.

Язык: Английский

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Cellular senescence in cancer: molecular mechanisms and therapeutic targets

MedComm, Год журнала: 2024, Номер 5(5)

Опубликована: Апрель 24, 2024

Abstract Aging exhibits several hallmarks in common with cancer, such as cellular senescence, dysbiosis, inflammation, genomic instability, and epigenetic changes. In recent decades, research into the role of senescence on tumor progression has received widespread attention. While how limits course cancer is well established, also been found to promote certain malignant phenotypes. The tumor‐promoting effect mainly elicited by a senescence‐associated secretory phenotype, which facilitates interaction senescent cells their surroundings. Targeting therefore offers promising technique for therapy. Drugs that pharmacologically restore normal function or eliminate them would assist reestablishing homeostasis cell signaling. Here, we describe its occurrence, impact biology. A “one‐two‐punch” therapeutic strategy first induced, followed use senotherapeutics eliminating introduced. advances application targeting treatment are outlined, an emphasis drug categories, strategies screening, design, efficient targeting. This work will foster thorough comprehension encourage additional within this field.

Язык: Английский

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Combined targeting of senescent cells and senescent macrophages: A new idea for integrated treatment of lung cancer

Seminars in Cancer Biology, Год журнала: 2024, Номер 106-107, С. 43 - 57

Опубликована: Авг. 29, 2024

Язык: Английский

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