<scp>ER</scp>
            ‐phagy: selective autophagy of the endoplasmic reticulum

Mochida, Keisuke; Nakatogawa, Hitoshi

doi:10.15252/embr.202255192

Cited by 44 publications

(25 citation statements)

References 115 publications

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“…A discovery we made during our research is that Bag3 has a role in monitoring the folding of newly synthesized proteins and guiding misfolded proteins towards refolding, depolymerization, or degradation [36][37][38]. It is well known that the ER is a protein processing factory in the cell and also plays a role in misfolded protein folding [39][40][41]. Given that chondrocytes are the sole cellular constituents of articular cartilage and are responsible for the synthesis and secretion of the collagen matrix within joints, Figures…”

Section: Discussionmentioning

confidence: 99%

Bag3 protects chondrocytes and alleviates osteoarthritis by restoring autophagy flux

Lin

et al. 2023

Preprint

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Objective Chondrocyte apoptosis resulting from the inhibition of autophagic flux is a significant contributor to Osteoarthritis (OA). In recent years, there has been increasing interest in the role of Bcl-2-associated athanogene 3 (Bag3) in autophagy; however, its specific contribution to the pathogenesis of knee osteoarthritis remains unclear.Methods X-ray imaging and tissue staining techniques were used to evaluate the radiographic and histomorphological features of the mouse knee joint. Western blotting was employed to analyze gene and protein expression levels in an in vitro setting. Immunofluorescence staining was utilized to identify and visualize specific proteins in the tissue samples. Knockdown and overexpression techniques were employed to manipulate the expression level of BAG3, a protein of interest. DMM (destabilization of the medial meniscus) was used to induce osteoarthritis in mice for studying the effects of Bag3 overexpression on OA development.Results The results of these experiments showed that in mouse knee OA tissue, BAG3 was upregulated compared to healthy tissue. Knockdown and overexpression experiments of BAG3 revealed a potential anti-apoptotic and autophagy-enhancing function of BAG3 in the context of osteoarthritis. CQ treatment reversed BAG3-induced chondrocyte protection under oxidative stress. Bag3 overexpression ameliorated DMM-induced OA development in mice.Conclusion Bag3 alleviates chondrocytes apoptosis by protecting autophagic flux, thereby improving OA.

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Section: Discussionmentioning

confidence: 99%

Bag3 protects chondrocytes and alleviates osteoarthritis by restoring autophagy flux

Lin

et al. 2023

Preprint

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“…ER stress-associated autophagy is essential for maintaining stabilized ER function via the degradation of aberrant and surplus components of the ER, as well as the damaged ER organelle itself, termed ER-phagy (Mochida and Nakatogawa 2022 ). ER-phagy targets the ER for degradation via fusion with the autophagosome when the ER is damaged or the acute response to the UPR exceeds the limit ( Figure 3 B).…”

Section: Crosstalk Between Er Stress and Autophagymentioning

confidence: 99%

Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases

Kwon

Kim

2023

Animal Cells and Systems

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Cells activate protective mechanisms to overcome stressful conditions that threaten cellular homeostasis, including imbalances in calcium, redox, and nutrient levels. Endoplasmic reticulum (ER) stress activates an intracellular signaling pathway, known as the unfolded protein response (UPR), to mitigate such circumstances and protect cells. Although ER stress is sometimes a negative regulator of autophagy, UPR induced by ER stress typically activates autophagy, a self-degradative pathway that further supports its cytoprotective role. Sustained activation of ER stress and autophagy is known to trigger cell death and is considered a therapeutic target for certain diseases. However, ER stress-induced autophagy can also lead to treatment resistance in cancer and exacerbation of certain diseases. Since the ER stress response and autophagy affect each other, and the degree of their activation is closely related to various diseases, understanding their relationship is very important. In this review, we summarize the current understanding of two fundamental cellular stress responses, the ER stress response and autophagy, and their crosstalk under pathological conditions to help develop therapies for inflammatory diseases, neurodegenerative disorders, and cancer.

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“…To remove the damaged ER by organellophagy (referred to as ER-phagy) [ 267 , 268 , 269 ], ATG39, ATG11, and ATG40 in yeast [ 270 ] and the family with sequence similarity 134, member B (FAM134B), and reticulon family proteins in mammals [ 271 , 272 , 273 ] serve as cargo receptors for targeting the stressed ER for degradation ( Figure 3 C). In addition, testis-expressed sequence 264 protein (TEX264) [ 274 , 275 ], Atlastins 3 (ATL3) [ 276 , 277 ], cell-cycle progression gene 1 (CCPG1) [ 278 ], translocon, SEC62 [ 279 ], and progesterone receptor membrane component 1 (PGRMC1) [ 280 ] act as cargo receptors of ER-phagy ( Figure 3 C).…”

Section: Autophagymentioning

confidence: 99%

Crosstalk between Autophagy and RLR Signaling

2023

Cells

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Autophagy plays a homeostatic role in regulating cellular metabolism by degrading unwanted intracellular materials and acts as a host defense mechanism by eliminating infecting pathogens, such as viruses. Upon viral infection, host cells often activate retinoic acid-inducible gene I (RIG-I)-like receptor (RLR) signaling to induce the transcription of type I interferons, thus establishing the first line of the innate antiviral response. In recent years, numerous studies have shown that virus-mediated autophagy activation may benefit viral replication through different actions on host cellular processes, including the modulation of RLR-mediated innate immunity. Here, an overview of the functional molecules and regulatory mechanism of the RLR antiviral immune response as well as autophagy is presented. Moreover, a summary of the current knowledge on the biological role of autophagy in regulating RLR antiviral signaling is provided. The molecular mechanisms underlying the crosstalk between autophagy and RLR innate immunity are also discussed.

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ER ‐phagy: selective autophagy of the endoplasmic reticulum

Cited by 44 publications

References 115 publications

Bag3 protects chondrocytes and alleviates osteoarthritis by restoring autophagy flux

Bag3 protects chondrocytes and alleviates osteoarthritis by restoring autophagy flux

Crosstalk between endoplasmic reticulum stress response and autophagy in human diseases

Crosstalk between Autophagy and RLR Signaling

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