Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

Guo, Jun; Huang, Xiuqing; Dou, Lin; Yan, Mingjing; Shen, Tao; Tang, Weiqing; Li, Jian

doi:10.1038/s41392-022-01251-0

Cited by 248 publications

(176 citation statements)

References 705 publications

(836 reference statements)

Supporting

Mentioning

160

Contrasting

Unclassified

Order By: Relevance

“…Guo et al, (2022) [ 33 ] have carefully explored the molecular mechanisms of aging and age-related diseases and their respective treatments and interventions. The study of the mechanisms of aging included various areas such as epigenetic regulation, proteostasis, autophagy, cellular senescence, and stem cells.…”

Section: Resultsmentioning

confidence: 99%

“…In other words, the study found that the concentration of autophagy-related proteins decreases in an individual with advancing age and that translocation to lysosomes is reduced, which promotes the aging of the organism. Furthermore, the researchers found much higher iron levels in senescent cells than in non-senescent or immortalized cells due to defective autophagic degradation of ferritin in lysosomes [ 33 ].…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Ferroptosis and Senescence: A Systematic Review

Coradduzza

Congiargiu

Chen

et al. 2023

IJMS

View full text Add to dashboard Cite

Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decay in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the aging process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death pathway characterized by excessive iron accumulation followed by the generation of reactive oxygen species (ROS). Oxidative stress is a common trigger of this condition and may be induced by various factors such as toxins, drugs, and inflammation. Ferroptosis is linked to numerous disorders, including cardiovascular disease, neurodegeneration, and cancer. Senescence is believed to contribute to the decay in tissue and organ functions occurring with aging. It has also been linked to the development of age-related pathologies, such as cardiovascular diseases, diabetes, and cancer. In particular, senescent cells have been shown to produce inflammatory cytokines and other pro-inflammatory molecules that can contribute to these conditions. In turn, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer. Ferroptosis is known to play a role in the development of these pathologies by promoting the death of damaged or diseased cells and contributing to the inflammation often associated. Both senescence and ferroptosis are complex pathways that are still not fully understood. Further research is needed to thoroughly investigate the role of these processes in aging and disease, and to identify potential interventions to target such processes in order to prevent or treat age-related conditions. This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, aging, and disease, and whether they can be exploited to block or limit the decay of the physiological functions in elderly people for a healthy longevity.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Ferroptosis and Senescence: A Systematic Review

Coradduzza

Congiargiu

Chen

et al. 2023

IJMS

View full text Add to dashboard Cite

show abstract

“…However, the study did not clarify whether ferroptosis is a process of autophagy activation or a prerequisite for it. Guo et al (2022) as well explored the molecular mechanism of aging and age-related diseases and their respective treatments and interventions. The study of the mechanisms of aging included various areas such as epigenetic regulation, proteostasis, autophagy, cellular senescence, and stem cells.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Ferroptosis and Senescence: A Systematic Review

Coradduzza¹,

Congiargiu²,

Chen³

et al. 2023

Preprint

View full text Add to dashboard Cite

Background: Senescence is a cellular ageing process in all multicellular organisms. It is characterized by a decline in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the ageing process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death characterized by excessive iron accumulation followed by the generation of reactive oxygen species (ROS). Oxidative stress is a common trigger of this condition and may be induced by various factors such as toxins, drugs, and inflammation. Ferroptosis is linked to numerous illnesses, including cardiovascular disease, neurodegeneration, and cancer. Relevance of these conditions to ageing and disease: Senescence is believed to contribute to the decline in tissue and organ function that occurs with ageing. It has also been linked to the development of age-related pathologies, such as cardiovascular diseases, diabetes, and cancer. In particular, senescent cells have been shown to produce inflammatory cytokines and other pro-inflammatory molecules that can contribute to these conditions. On the other hand, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer [1]. It is known to play a role in developing these diseases by promoting the death of damaged or diseased cells and contributing to the inflammation often associated with them. Both senescence and ferroptosis are complex processes that are still not fully understood. Further research is needed to thoroughly understand the role of these processes in ageing and disease, and to identify potential interventions to target these processes to prevent or treat age-related conditions. Objectives: This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, ageing, and disease.

show abstract

“…Cell aging refers to a cell state implicated in a wide spectrum of physiological processes and could be targeted to slow the aging process [23,24]. Unfolded protein response, proteolytic processing by proteases, cell proliferation and transmembrane transport were all profoundly modulated the cellular senescence and thus age-related diseases [25][26][27][28].…”

Section: Discussionmentioning

confidence: 99%

EIF5A2 specifically regulates the transcription of aging-related genes in human neuroblastoma cells

Liu

Chen

et al. 2023

BMC Geriatr

View full text Add to dashboard Cite

Background Post-transcriptional regulation plays a critical role in controlling biological processes such as aging. Previous studies have shown that eukaryotic initiation factor 5A (EIF5A) might play a crucial role in aging. It is unknown whether EIF5A2, a second isoform of EIF5A, could impact aging through post-transcriptional regulation. Methods In the present study, EIF5A2 overexpression (EIF5A2-OE) was induced in SH-SY5Y cells. RNA-seq, bioinformatics analysis and RT-qPCR validation experiments were then performed to explore the molecular mechanism of EIF5A2-mediated transcriptional regulation. Cell viability, proportion of senescent cells and the cell cycle were respectively determined by Cell Counting Kit-8, SA-β‑galactosidase and flow cytometry to evaluate the cell senescence. Results A total of 190 downregulated and 126 upregulated genes related to EIF5A2-OE were identified. Genes closely related to cellular aging processes such as unfolded protein response (UPR), cell adhesion and calcium signaling pathway were under global transcriptional regulation. Moreover, EIF5A2-OE promoted the viability of SH-SY5Y cells and reduced cell senescence in vitro. Among 30 genes with the most significant expression differences in EIF5A2-OE cells, we identified eight genes, including ASNS, ATF3, ATF4, CEBPB, DDIT3, HERPUD1, HSPA5 and XBP1, enriched in the UPR. Through EIF5A2-tanscription factors (TFs)-targets regulation network in EIF5A2-OE cells, we found three TFs, BHLHE40, RHOXF1 and TBX20, that targeted at these eight UPR-related genes. Verification test via the published database of human glial cell tissue showed only BHLHE40 and RHOXF1 were significantly associated with EIF5A2. Conclusions Our findings suggest that EIF5A2 may alleviate cell senescence in vitro and mediate UPR-related genes via specific TFs. Thus, EIF5A2 could function as a regulator of aging via the regulation of transcription, which greatly expands the current understanding of the mechanisms of EIF5A2-mediated gene regulation.

show abstract

Aging and aging-related diseases: from molecular mechanisms to interventions and treatments

Cited by 248 publications

References 705 publications

Ferroptosis and Senescence: A Systematic Review

Ferroptosis and Senescence: A Systematic Review

Ferroptosis and Senescence: A Systematic Review

EIF5A2 specifically regulates the transcription of aging-related genes in human neuroblastoma cells

Contact Info

Product

Resources

About