Autophagy receptors as viral targets

Ylä-Anttila, Päivi

doi:10.1186/s11658-021-00272-x

Cited by 17 publications

(10 citation statements)

References 53 publications

(68 reference statements)

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“…Autophagy is an intracellular degradation system that regulates energy metabolism, degrades impaired proteins, and maintains body homeostasis; it has been shown to restore the function of damaged chondrocytes, alleviating OA progression by protecting articular cartilage [ 22 – 24 ]. Mitochondria are the organelle sites for tricarboxylic acid cycle (TCA) progression and supply the electron transport chain (ETC) to manage energy production and cell distribution [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage

Jin

Jiang

et al. 2022

Cell Mol Biol Lett

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Osteoarthritis (OA) is a widespread chronic degenerative joint disease characterized by the degeneration of articular cartilage or inflamed joints. Our findings indicated that treatment with artemisinin (AT) downregulates the protein levels of MMP3, MMP13, and ADAMTS5, which are cartilage degradation-related proteins in OA, and inhibits the expression of inflammatory factors in interleukin-1β (IL-1β)-stimulated chondrocytes. However, the mechanism of the role of AT in OA remains unclear. Here, we performed gene sequencing and bioinformatics analysis in control, OA, and OA + AT groups to demonstrate that several mRNA candidates were enriched in the PI3K/AKT/mTOR signaling pathway, and TNFSF11 was significantly downregulated after AT treatment. TNFSF11 was downregulated in the OA + AT group, whereas it was upregulated in rat OA tissues and OA chondrocytes. Therefore, we confirmed that TNFSF11 was the target gene of AT. In addition, our study revealed that AT relieved cartilage degradation and defection by activating mitochondrial autophagy via inhibiting the PI3K/AKT/mTOR signaling pathway in IL-1β-induced chondrocytes. Furthermore, an OA model was established in rats with medial meniscus destabilization. Injecting AT into the knee joints of OA rat alleviated surgical resection-induced cartilage destruction. Thus, these findings revealed that AT relieves OA by activating mitochondrial autophagy by reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling.

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Section: Introductionmentioning

confidence: 99%

Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage

Jin

Jiang

et al. 2022

Cell Mol Biol Lett

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“…In addition to maintaining cellular homeostasis, autophagy also participates in pathogen clearance. Selective autophagy of intracellular pathogens is called xenophagy, while that of virions or viral components is known as virophagy ( Yla-Anttila, 2021 ). Selective autophagy depends on receptor recognition of cargo and the initiation of autophagosome formation ( Huang et al., 2020 ; Vo and Choi, 2021 ).…”

Section: Autophagy Machinerymentioning

confidence: 99%

Clearance or Hijack: Universal Interplay Mechanisms Between Viruses and Host Autophagy From Plants to Animals

Luo

Ren

2022

Front. Cell. Infect. Microbiol.

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Viruses typically hijack the cellular machinery of their hosts for successful infection and replication, while the hosts protect themselves against viral invasion through a variety of defense responses, including autophagy, an evolutionarily ancient catabolic pathway conserved from plants to animals. Double-membrane vesicles called autophagosomes transport trapped viral cargo to lysosomes or vacuoles for degradation. However, during an ongoing evolutionary arms race, viruses have acquired a strong ability to disrupt or even exploit the autophagy machinery of their hosts for successful invasion. In this review, we analyze the universal role of autophagy in antiviral defenses in animals and plants and summarize how viruses evade host immune responses by disrupting and manipulating host autophagy. The review provides novel insights into the role of autophagy in virus–host interactions and offers potential targets for the prevention and control of viral infection in both plants and animals.

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“…In addition, chloroquine is a well-known inhibitor of autophagy that inhibits binding of autophagosomes to vesicles bearing lysosomal enzymes. Autophagy is considered as a part of the innate immunity against viral infections [ 98 ].…”

Section: Drugs Inhibiting Virus Entry To Host Cellsmentioning

confidence: 99%

COVID-19 therapies: do we see substantial progress?

et al. 2022

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The appearance of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and its spread all over the world is the cause of the coronavirus disease 2019 (COVID-19) pandemic, which has recently resulted in almost 400 million confirmed cases and 6 million deaths, not to mention unknown long-term or persistent side effects in convalescent individuals. In this short review, we discuss approaches to treat COVID-19 that are based on current knowledge of the mechanisms of viral cell receptor recognition, virus–host membrane fusion, and inhibition of viral RNA and viral assembly. Despite enormous progress in antiviral therapy and prevention, new effective therapies are still in great demand.

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Autophagy receptors as viral targets

Cited by 17 publications

References 53 publications

Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage

Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage

Clearance or Hijack: Universal Interplay Mechanisms Between Viruses and Host Autophagy From Plants to Animals

COVID-19 therapies: do we see substantial progress?

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