Autophagy drives fibroblast senescence through MTORC2 regulation

Bernard, Monique; Yang, Bing; Migneault, Francis; Turgeon, Julie; Dieudé, Mélanie; Olivier, Marc-Alexandre; Cardin, Guillaume B.; El-Diwany, Mostafa; Underwood, Katy; Rodier, Françis; Hébert, Marie‐Josée

doi:10.1080/15548627.2020.1713640

Cited by 110 publications

(85 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, mTORC2 activity is also sensitive to the redox state [ 134 ]. ROS and starvation combine increase mTORC2 signaling, leading to long-term cell cycle arrest, senescence, or differentiation [ 135 ] ( Fig. 3 ).…”

Section: The Relationship Between Reactive Oxygen Species and Autophamentioning

confidence: 99%

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

et al. 2020

View full text Add to dashboard Cite

The autophagic pathway involves the encapsulation of substrates in double-membraned vesicles, which are subsequently delivered to the lysosome for enzymatic degradation and recycling of metabolic precursors. Autophagy is a major cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of reactive oxygen species (ROS), leading to oxidative stress and the associated oxidative damage of cellular components. Accumulating evidence indicates that autophagy is necessary to maintain redox homeostasis. ROS activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular damaged macromolecules and dysfunctional organelles. The cellular responses triggered by oxidative stress include the altered regulation of signaling pathways that culminate in the regulation of autophagy. Current research suggests a central role for autophagy as a mammalian oxidative stress response and its interrelationship to other stress defense systems. Altered autophagy phenotypes have been observed in lung diseases such as chronic obstructive lung disease, acute lung injury, cystic fibrosis, idiopathic pulmonary fibrosis, and pulmonary arterial hypertension, and asthma. Understanding the mechanisms by which ROS regulate autophagy will provide novel therapeutic targets for lung diseases. This review highlights our current understanding on the interplay between ROS and autophagy in the development of pulmonary disease.

show abstract

Section: The Relationship Between Reactive Oxygen Species and Autophamentioning

confidence: 99%

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Altogether, mediated by mTOR activity, aging influenced the response of lung fibroblasts to autophagy and enhanced the vulnerability to lung fibrosis 105 . More recent studies reported that sustained autophagy promoted fibroblast senescence and prevented the differentiation of fibroblasts to myofibroblasts through the regulation of mTOR complex 2 (mTORC2) 106 . However, decreased degradation of p62 and impaired autophagy flux were also observed in senescent cells 107 .…”

Section: Lung Fibrosis and Autophagymentioning

confidence: 99%

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Liu¹,

Wu²,

Li³

2020

Theranostics

View full text Add to dashboard Cite

Fibrosis occurs in most human organs including the liver, lung, heart and kidney, and is crucial for the progression of most chronic diseases. As an indispensable catabolic process for intracellular quality control and homeostasis, autophagy occurs in most mammalian cells and is implicated in many biological processes including fibrogenesis. Although advances have been made in understanding autophagy process, the potential role of autophagy in fibrotic diseases remains controversial and has recently attracted a great deal of attention. In the current review, we summarize the commonalities of autophagy affecting different types of fibrosis in different organs, including the liver, lung, heart, and kidney as well as in cystic fibrosis, systematically outline the contradictory results and highlight the distinct role of autophagy during the various stages of fibrosis. In summary, the exact role autophagy plays in fibrogenesis depends on specific cell types and different stimuli, and identifying and evaluating the pathogenic contribution of autophagy in fibrogenesis will promote the discovery of novel therapeutic strategies for the clinical management of these fibrotic diseases.

show abstract

“…Then, the specific molecular mechanism of CDR1 as/miR-7 in the regulation of autophagy in breast cancer stem cells was further investigated. We observed that CDR1as-7/miR-7 modulated distinct steps of autophagy in breast cancer stem cells by targeting autophagy-related genes, including LKB1, ATG4A and ATG7, which act at distinct steps of autophagy (Bernard et al 2020). Tumor suppressor gene LKB1 serves as the upstream molecule controlling AMPK activation.…”

Section: Discussionmentioning

confidence: 95%

Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44⁺/CD24^- phenotype breast cancer stem cells in vitro

Dong

Chen

et al. 2021

All Life

View full text Add to dashboard Cite

Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44 + /CD24 phenotype breast cancer stem cells in vitro Zhi-qiang Ye, Xu-bin Dong, Han-bin Chen, Dian-na Gu & Zheng-jun Qiu To cite this article: Zhi-qiang Ye, Xu-bin Dong, Han-bin Chen, Dian-na Gu & Zheng-jun Qiu (2021) Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44 + /CD24 phenotype breast cancer stem cells invitro,

show abstract

Autophagy drives fibroblast senescence through MTORC2 regulation

Cited by 110 publications

References 56 publications

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44⁺/CD24^- phenotype breast cancer stem cells in vitro

Contact Info

Product

Resources

About

Autophagy drives fibroblast senescence through MTORC2 regulation

Cited by 110 publications

References 56 publications

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

Self-eating: friend or foe? The emerging role of autophagy in fibrotic diseases

Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44+/CD24- phenotype breast cancer stem cells in vitro

Contact Info

Product

Resources

About

Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44⁺/CD24^- phenotype breast cancer stem cells in vitro