Ageing, cellular senescence and chronic kidney disease: experimental evidence

Tan, Huishi; Xu, Jie; Liu, Youhua

doi:10.1097/mnh.0000000000000782

Cited by 24 publications

(17 citation statements)

References 94 publications

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“…The proinflammatory and profibrotic features of failed-repair PTCs are in good agreement with the senescence- associated secretory phenotype (SASP) reported in aged and injured nonkidney tissues [38]. Cellular senescence is involved in the pathogenesis of chronic kidney disease and senescence-targeting interventions displayed beneficial role in animal models of kidney ageing and disease [60,61 ▪ ,62,63]. However, the role of some features of cellular senescence in other systems has been controversial in the biology of failed-repair, in particular the role of cell cycle arrest.…”

Section: Altered Proximal Tubule Cells In Failed Tubule Repairsupporting

confidence: 71%

Proximal tubule responses to injury: interrogation by single-cell transcriptomics

Cippà

McMahon

2023

Current Opinion in Nephrology &Amp; Hypertension

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Purpose of reviewAcute kidney injury (AKI) occurs in approximately 10--15% of patients admitted to hospital and is associated with adverse clinical outcomes. Despite recent advances, management of patients with AKI is still mainly supportive, including the avoidance of nephrotoxins, volume and haemodynamic management and renal replacement therapy. A better understanding of the renal response to injury is the prerequisite to overcome current limitations in AKI diagnostics and therapy. Recent findingsSingle-cell technologies provided new opportunities to study the complexity of the kidney and have been instrumental for rapid advancements in the understanding of the cellular and molecular mechanisms of AKI.

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Section: Altered Proximal Tubule Cells In Failed Tubule Repairsupporting

confidence: 71%

Proximal tubule responses to injury: interrogation by single-cell transcriptomics

Cippà

McMahon

2023

Current Opinion in Nephrology &Amp; Hypertension

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“…However, the mortality of CKD patients is still high, and their life quality is low. Since senescence plays an important role in CKD, it could be Frontiers in Pharmacology frontiersin.org assumed as a new target for CKD treatment (Tan et al, 2022). The approach of targeting senescence is known as senotherapy, which mainly includes senolytics, senomorphics, and rejuvenating agents (Goligorsky, 2020).…”

Section: Targeting Renal Senescence In Therapy Of Ckdmentioning

confidence: 99%

“…Renal senescence and CKD share common characteristics and mechanisms, and there is a complex interactive relationship between them (Figure 4). Renal senescence is a promising target for therapeutic intervention of CKD, as preclinical data have shown the efficacy of senotherapies (Tan et al, 2022). In the future, more effective senotherapies and their judicious implementation are expected to fight against the progression of CKD or even reverse CKD, however, several challenges remained.…”

Section: Future Prospectsmentioning

confidence: 99%

The interaction between cellular senescence and chronic kidney disease as a therapeutic opportunity

Zhao

Qiao²,

Mao

et al. 2022

Front. Pharmacol.

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Chronic kidney disease (CKD) is an increasingly serious public health problem in the world, but the effective therapeutic approach is quite limited at present. Cellular senescence is characterized by the irreversible cell cycle arrest, senescence-associated secretory phenotype (SASP) and senescent cell anti-apoptotic pathways (SCAPs). Renal senescence shares many similarities with CKD, including etiology, mechanism, pathological change, phenotype and outcome, however, it is difficult to judge whether renal senescence is a trigger or a consequence of CKD, since there is a complex correlation between them. A variety of cellular signaling mechanisms are involved in their interactive association, which provides new potential targets for the intervention of CKD, and then extends the researches on senotherapy. Our review summarizes the common features of renal senescence and CKD, the interaction between them, the strategies of senotherapy, and the open questions for future research.

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“…Moreover, other researchers confirmed that inhibition of tubular DNA damage and senescence could attenuate renal interstitial fibrosis after AKI, which was the key point of AKI progression to chronic kidney disease (CKD) [ 21 ]. In addition, senescent cells produce a complex secretome, known as the senescence-associated secretory phenotype (SASP), which promotes inflammation and the development of CKD [ 22 ]. Therefore, the removal of senescent cells by activating apoptosis appears to be a key mechanism for treating AKI and preventing the progression of CKD.…”

Section: Introductionmentioning

confidence: 99%

β-Cryptoxanthin Maintains Mitochondrial Function by Promoting NRF2 Nuclear Translocation to Inhibit Oxidative Stress-Induced Senescence in HK-2 Cells

Zhang

Mao

et al. 2023

IJMS

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The mechanisms of acute kidney injury and chronic kidney disease remain incompletely revealed, and drug development is a pressing clinical challenge. Oxidative stress-induced cellular senescence and mitochondrial damage are important biological events in a variety of kidney diseases. As a type of carotenoid, β-Cryptoxanthin (BCX) has various biological functions, which means it is a potential therapeutic candidate for the treatment of kidney disease. However, the role of BCX in the kidney is unclear, and the effect of BCX on oxidative stress and cellular senescence in renal cells is also unknown. Therefore, we conducted a series of studies on human renal tubular epithelial (HK-2) cells in vitro. In the present study, we investigated the effect of BCX pretreatment on H2O2-induced oxidative stress and cellular senescence and explored the potential mechanism of BCX action. The results showed that BCX attenuated H2O2-induced oxidative stress and cellular senescence in HK-2 cells. Moreover, BCX promoted NRF2 nuclear expression, maintained mitochondrial function, and reduced mitochondrial damage in HK-2 cells. In addition, silencing NRF2 altered the protective effect of BCX on mitochondria and significantly reversed the anti-oxidative stress and anti-senescence effects of BCX in HK-2 cells. We concluded that BCX maintained mitochondrial function by promoting NRF2 nuclear translocation to inhibit oxidative stress-induced senescence in HK-2 cells. In light of these findings, the application of BCX might be a promising strategy for the prevention and treatment of kidney diseases.

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Ageing, cellular senescence and chronic kidney disease: experimental evidence

Cited by 24 publications

References 94 publications

Proximal tubule responses to injury: interrogation by single-cell transcriptomics

Proximal tubule responses to injury: interrogation by single-cell transcriptomics

The interaction between cellular senescence and chronic kidney disease as a therapeutic opportunity

β-Cryptoxanthin Maintains Mitochondrial Function by Promoting NRF2 Nuclear Translocation to Inhibit Oxidative Stress-Induced Senescence in HK-2 Cells

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