To target cellular senescence in diabetic kidney disease: the known and the unknown DOI Creative Commons

Yuehan Wei,

Shan Mou, Qing Yang

et al.

Clinical Science, Journal Year: 2024, Volume and Issue: 138(16), P. 991 - 1007

Published: Aug. 1, 2024

Abstract Cellular senescence represents a condition of irreversible cell cycle arrest, characterized by heightened senescence-associated beta-galactosidase (SA-β-Gal) activity, secretory phenotype (SASP), and activation the DNA damage response (DDR). Diabetic kidney disease (DKD) is significant contributor to end-stage renal (ESRD) globally, with ongoing unmet needs in terms current treatments. The role pathogenesis DKD has attracted substantial attention evidence premature this condition. process cellular appears be associated mitochondrial redox pathways, autophagy, endoplasmic reticulum (ER) stress. Increasing accumulation senescent cells diabetic not only leads an impaired capacity for repair injury, but also secretion pro-inflammatory profibrotic cytokines growth factors causing inflammation fibrosis. Current treatments diabetes exhibit varying degrees renoprotection, potentially via mitigation kidney. Targeting clearance through pharmaceutical interventions could emerge as promising strategy preventing treating DKD. In paper, we review understanding summarize possible therapeutic relevant field.

Language: Английский

Therapy-induced senescence is a transient drug resistance mechanism in breast cancer. DOI

Eszter Bajtai,

Csaba Kiss, Éva Bakos

et al.

PubMed, Journal Year: 2025, Volume and Issue: 24(1), P. 128 - 128

Published: May 1, 2025

Language: Английский

Citations

0
Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management DOI Creative Commons

Paige Charlotte Alison Phillips,

Mafalda de Sousa Loreto Aresta Branco,

Chelsy L. Cliff

et al.

Diabetic Medicine, Journal Year: 2024, Volume and Issue: unknown

Published: July 12, 2024

Abstract Background/Aims As a microvascular complication, diabetic kidney disease is the leading cause of chronic and end‐stage renal worldwide. While underlying pathophysiology driving transition to failure yet be fully understood, recent studies suggest that cellular senescence central in development progression. Consequently, understanding molecular mechanisms which initiate drive response milieu crucial developing targeted therapies halt progression disease. Methods To understand mechanistic pathways underpinning context disease, we reviewed literature using PubMed for English language articles contained key words related senescence, inflammation, fibrosis, senescence‐associated secretory phenotype (SASP), autophagy, diabetes. Results Aberrant accumulation metabolically active senescent cells notable event Through autocrine‐ paracrine‐mediated mechanisms, resident potentiate inflammation fibrosis through increased expression secretion pro‐inflammatory cytokines, chemoattractants, recruitment immune cells, myofibroblast activation, extracellular matrix remodelling. Compounds eliminate and/or target SASP – including senolytic senomorphics drugs demonstrate promising results reducing cell burden associated effect. Conclusions Here evidence link between highlight potential therapeutic targets could exploited delay improve outcomes individuals with Trials are now required translate their clinical setting.

Language: Английский

Citations

3
To target cellular senescence in diabetic kidney disease: the known and the unknown DOI Creative Commons

Yuehan Wei,

Shan Mou, Qing Yang

et al.

Clinical Science, Journal Year: 2024, Volume and Issue: 138(16), P. 991 - 1007

Published: Aug. 1, 2024

Abstract Cellular senescence represents a condition of irreversible cell cycle arrest, characterized by heightened senescence-associated beta-galactosidase (SA-β-Gal) activity, secretory phenotype (SASP), and activation the DNA damage response (DDR). Diabetic kidney disease (DKD) is significant contributor to end-stage renal (ESRD) globally, with ongoing unmet needs in terms current treatments. The role pathogenesis DKD has attracted substantial attention evidence premature this condition. process cellular appears be associated mitochondrial redox pathways, autophagy, endoplasmic reticulum (ER) stress. Increasing accumulation senescent cells diabetic not only leads an impaired capacity for repair injury, but also secretion pro-inflammatory profibrotic cytokines growth factors causing inflammation fibrosis. Current treatments diabetes exhibit varying degrees renoprotection, potentially via mitigation kidney. Targeting clearance through pharmaceutical interventions could emerge as promising strategy preventing treating DKD. In paper, we review understanding summarize possible therapeutic relevant field.

Language: Английский

Citations

3