Cellular senescence in ischemia/reperfusion injury

Chen, Chaojin; Zheng, Muxu; Hou, Hongbiao; Fang, Sijian; Chen, Liubing; Yang, Jing; Yao, Weifeng; Zhang, Qi; Hei, Ziqing

doi:10.1038/s41420-022-01205-z

Cited by 12 publications

(8 citation statements)

References 144 publications

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“…Similarly, human Muse cells were found to survive for 4 weeks in chemically induced Hunner-type interstitial cystitis-like rats [65]. The harsh microenvironment of lung ischemia-reperfusion (IR) injury contains both proapoptotic and pro-inflammatory cytokines and reactive oxygen species [97,98]. In a study of acute lung ischemia-reperfusion (IR) injury in a rat model, the results showed that human Muse cells were more effective at homing into damaged lung tissue, inhibiting apoptosis and promoting proliferation of host alveolar cells than MSCs [64].…”

Section: Superior Survivability In Vivomentioning

confidence: 99%

“…Muse cells were more abundant in lung tissue from ischemia-reperfusion injury compared to MSCs. Human Muse cells secreted beneficial substances (KGF, HGF, Ang-1 and PGE 2) in vitro, and it is possible that these protective factors together exert tissue repair, apoptosis prevention and alveolar fluid clearance [64,97,98]. Muse cells also have therapeutic potential for osteochondral repair [68].…”

Section: The Role Of Muse Cells In Another Disease (Including Lung In...mentioning

confidence: 99%

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Multilineage-Differentiating Stress-Enduring Cells: A Powerful Tool for Tissue Damage Repair

Que,

Mai,

et al. 2024

Preprint

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Multilineage-differentiating stress-enduring (Muse) cells, a cell subgroup from mesenchymal stem cells (MSCs), are pluripotent cells with unique characteristics such as non-tumorigenic and pluripotent differentiation ability. After homing, Muse cells spontaneously differentiate into tissue component cells and supplement damaged/lost cells to participate in tissue repair. Importantly, Muse cells can survive in injured tissue for an extended period, stabilizing and promoting tissue repair. In addition, it has been confirmed that injection of exogenous Muse cells exerts anti-inflammatory, anti-apoptosis, anti-fibrosis, immunomodulatory, and paracrine protective effects in vivo. The discovery of Muse cells is an important breakthrough in regenerative medicine. The article provides a comprehensive review of the characteristics, sources, and potential mechanisms of Muse cells for tissue repair and regeneration. This review serves as a foundation for the further utilization of Muse cells as a key clinical tool in regenerative medicine.

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Section: Superior Survivability In Vivomentioning

confidence: 99%

Section: The Role Of Muse Cells In Another Disease (Including Lung In...mentioning

confidence: 99%

Multilineage-Differentiating Stress-Enduring Cells: A Powerful Tool for Tissue Damage Repair

Que,

Mai,

et al. 2024

Preprint

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“…There are different critical care scenarios where an increase of the senescent response has been observed. A widely studied trigger is ischemia/reperfusion injury [ 16 ], which refers to the damage caused by a temporary lack of blood supply followed by its restoration. This critical situation commonly occurs in emergency surgery, organ transplantation, and cardiovascular events.…”

Section: Activation Of Senescence In Critical Illnessmentioning

confidence: 99%

Activation of senescence in critically ill patients: mechanisms, consequences and therapeutic opportunities

Martín-Vicente,

López-Martínez,

Rioseras

et al. 2024

Ann. Intensive Care

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Whereas aging is a whole-organism process, senescence is a cell mechanism that can be triggered by several stimuli. There is increasing evidence that critical conditions activate cell senescence programs irrespective of patient’s age. In this review, we briefly describe the basic senescence pathways and the consequences of their activation in critically ill patients. The available evidence suggests a paradigm in which activation of senescence can be beneficial in the short term by rendering cells resistant to apoptosis, but also detrimental in a late phase by inducing a pro-inflammatory and pro-fibrotic state. Senescence can be a therapeutic target. The use of drugs that eliminate senescent cells (senolytics) or the senescence-associated phenotype (senomorphics) will require monitoring of these cell responses and identification of therapeutic windows to improve the outcome of critically ill patients.

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“…The lack of blood flow deprives the tissue of oxygen and nutrients, leading to a state of hypoxia and nutrient deprivation. This can result in cellular dysfunction and, if prolonged, irreversible cell damage and death [ 325 ]. The subsequent reperfusion stage is necessary to deliver oxygen and nutrients to the ischemic tissue, however, it paradoxically leads to further tissue damage.…”

Section: Ferroptosis In Pathologiesmentioning

confidence: 99%

The mechanism of ferroptosis and its related diseases

Feng,

Tang,

Wang

et al. 2023

Mol Biomed

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Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation of lipid peroxides, provides a novel avenue for delving into the intersection of cellular metabolism, oxidative stress, and disease pathology. We have witnessed a mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological and pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, and traumatic tissue injuries. By unraveling the intricate underpinnings of the molecular machinery, pivotal contributors, intricate signaling conduits, and regulatory networks governing ferroptosis, researchers aim to bridge the gap between the intricacies of this unique mode of cellular death and its multifaceted implications for health and disease. In light of the rapidly advancing landscape of ferroptosis research, we present a comprehensive review aiming at the extensive implications of ferroptosis in the origins and progress of human diseases. This review concludes with a careful analysis of potential treatment approaches carefully designed to either inhibit or promote ferroptosis. Additionally, we have succinctly summarized the potential therapeutic targets and compounds that hold promise in targeting ferroptosis within various diseases. This pivotal facet underscores the burgeoning possibilities for manipulating ferroptosis as a therapeutic strategy. In summary, this review enriched the insights of both investigators and practitioners, while fostering an elevated comprehension of ferroptosis and its latent translational utilities. By revealing the basic processes and investigating treatment possibilities, this review provides a crucial resource for scientists and medical practitioners, aiding in a deep understanding of ferroptosis and its effects in various disease situations.

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Cellular senescence in ischemia/reperfusion injury

Cited by 12 publications

References 144 publications

Multilineage-Differentiating Stress-Enduring Cells: A Powerful Tool for Tissue Damage Repair

Multilineage-Differentiating Stress-Enduring Cells: A Powerful Tool for Tissue Damage Repair

Activation of senescence in critically ill patients: mechanisms, consequences and therapeutic opportunities

The mechanism of ferroptosis and its related diseases

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