Lactylation: A Novel Epigenetic Regulator of Cellular Senescence DOI Creative Commons
Caiyu Sun, Jiaxuan Li, Lei Dong

et al.

Aging and Disease, Journal Year: 2025, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2025

Cellular senescence is the basic unit of organismal aging, a complicated biological process involving several cell types and tissues. It also an important mechanism by which body responds to damage potential carcinogenesis. However, excessive or abnormal cellular can lead tissue functional degradation occurrence diseases. In recent years, role epigenetic modifications in has received extensive attention. Lactylation, novel post-translational modification derived from lactate, recently gained significant attention as key factor metabolism regulation, gradually demonstrating its importance regulation senescence. This review emphasizes bidirectional causal relationship between lactylation senescence, highlighting therapeutic target for aging-related

Language: Английский

TRAP1 drives smooth muscle cell senescence and promotes atherosclerosis via HDAC3-primed histone H4 lysine 12 lactylation DOI Creative Commons
Xuesong Li, Minghong Chen,

Xiang Chen

et al.

European Heart Journal, Journal Year: 2024, Volume and Issue: 45(39), P. 4219 - 4235

Published: Aug. 1, 2024

Vascular smooth muscle cell (VSMC) senescence is crucial for the development of atherosclerosis, characterized by metabolic abnormalities. Tumour necrosis factor receptor-associated protein 1 (TRAP1), a regulator associated with ageing, might be implicated in atherosclerosis. As role TRAP1 atherosclerosis remains elusive, this study aimed to examine function VSMC and

Language: Английский

Citations

30
Arterial Stiffness: From Basic Primers to Integrative Physiology DOI Creative Commons
Véronique Regnault, Patrick Lacolley, Stéphane Laurent

et al.

Annual Review of Physiology, Journal Year: 2024, Volume and Issue: 86(1), P. 99 - 121

Published: Feb. 12, 2024

The elastic properties of conductance arteries are one the most important hemodynamic functions in body, and data continue to emerge regarding importance their dysfunction vascular aging a range cardiovascular diseases. Here, we provide new insight into integrative physiology arterial stiffening its clinical consequence. We also comprehensively review progress made on pathways/molecules that appear today as basic determinants stiffness, particularly those mediating smooth muscle cell (VSMC) contractility, plasticity stiffness. focus membrane nuclear mechanotransduction, clearance function wall, phenotypic switching VSMCs, immunoinflammatory stimuli epigenetic mechanisms. Finally, discuss advances latest studies revisit classical therapeutic concepts stiffness lead patient-by-patient strategy according risk exposure underlying disease.

Language: Английский

Citations

19
Mitochondrial dysfunction and its association with age-related disorders DOI Creative Commons
Indumathi Somasundaram,

Samatha M. Jain,

Marcel Blot-Chabaud

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: July 2, 2024

Aging is a complex process that features functional decline in many organelles. Various factors influence the aging process, such as chromosomal abnormalities, epigenetic changes, telomere shortening, oxidative stress, and mitochondrial dysfunction. Mitochondrial dysfunction significantly impacts because mitochondria regulate cellular energy, balance, calcium levels. integrity maintained by mitophagy, which helps maintain homeostasis, prevents ROS production, protects against mtDNA damage. However, increased uptake stress can disrupt membrane potential permeability, leading to apoptotic cascade. This disruption causes production of free radicals, modification accumulation DNA mutations, contribute aging. dysfunction, resulting from structural linked age-related degenerative diseases. review focuses on its implications disorders, anti-aging strategies through targeting

Language: Английский

Citations

17
Redox regulation: mechanisms, biology and therapeutic targets in diseases DOI Creative Commons
Bowen Li, Hui Ming, Siyuan Qin

et al.

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

Published: March 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.

Language: Английский

Citations

4
Escape from senescence: molecular basis and therapeutic ramifications DOI Creative Commons
Konstantinos Evangelou, Konstantinos Belogiannis, Angelos Papaspyropoulos

et al.

The Journal of Pathology, Journal Year: 2023, Volume and Issue: 260(5), P. 649 - 665

Published: Aug. 1, 2023

Abstract Cellular senescence constitutes a stress response mechanism in reaction to plethora of stimuli. Senescent cells exhibit cell‐cycle arrest and altered function. While withdrawal has been perceived as permanent, recent evidence cancer research introduced the so‐called escape‐from‐senescence concept. In particular, under certain conditions, senescent may resume proliferation, acquiring highly aggressive features. As such, they have associated with tumour relapse, rendering less effective inhibiting progression. Thus, conventional treatments, incapable eliminating senescence, benefit if revisited include senolytic agents. To this end, it is anticipated that assessment burden everyday clinical material by pathologists will play crucial role near future, laying foundation for more personalised approaches. Here, we provide an overview investigations phenomenon, identified mechanisms, well major implications pathology therapy. © 2023 The Authors. Journal Pathology published John Wiley & Sons Ltd on behalf Pathological Society Great Britain Ireland.

Language: Английский

Citations

28
A fluorophore-conjugated reagent enabling rapid detection, isolation and live tracking of senescent cells DOI Creative Commons

Sophia Magkouta,

Dimitris Veroutis,

Athanasios Pousias

et al.

Molecular Cell, Journal Year: 2023, Volume and Issue: 83(19), P. 3558 - 3573.e7

Published: Oct. 1, 2023

Language: Английский

Citations

25
Epigenetic regulations of cellular senescence in osteoporosis DOI
Shaochuan Huo,

Xinzheng Tang,

Weijian Chen

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 99, P. 102235 - 102235

Published: Feb. 16, 2024

Language: Английский

Citations

17
Examining the wound healing potential of curcumin-infused electrospun nanofibers from polyglutamic acid and gum arabic DOI

Cuilin Cheng,

Rongchun Wang, Jiapei Ma

et al.

International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 267, P. 131237 - 131237

Published: March 28, 2024

Language: Английский

Citations

15
Neutrophil extracellular traps and long COVID DOI Creative Commons
Areez Shafqat, Mohamed H. Omer, Ibrahem Albalkhi

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Sept. 27, 2023

Post-acute COVID-19 sequelae, commonly known as long COVID, encompasses a range of systemic symptoms experienced by significant number survivors. The underlying pathophysiology COVID has become topic intense research discussion. While chronic inflammation in received considerable attention, the role neutrophils, which are most abundant all immune cells and primary responders to inflammation, been unfortunately overlooked, perhaps due their short lifespan. In this review, we discuss emerging neutrophil extracellular traps (NETs) persistent inflammatory response observed patients. We present early evidence linking persistence NETs pulmonary fibrosis, cardiovascular abnormalities, neurological dysfunction COVID. Several uncertainties require investigation future studies. These include mechanisms SARS-CoV-2 brings about sustained activation phenotypes after infection resolution; whether heterogeneity neutrophils seen acute persists into phase; presence autoantibodies can induce protect them from degradation; exert differential, organ-specific effects; specifically NET components contribute pathologies, such fibrosis; senescent drive formation through pro-inflammatory secretome Answering these questions may pave way for development clinically applicable strategies targeting NETs, providing relief health crisis.

Language: Английский

Citations

23
PM2.5-mediated cardiovascular disease in aging: Cardiometabolic risks, molecular mechanisms and potential interventions DOI Creative Commons

Francis Chanda,

Kai-Xuan Lin,

Abdallah Iddy Chaurembo

et al.

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 954, P. 176255 - 176255

Published: Sept. 12, 2024

Language: Английский

Citations

7