Autophagy and Mitochondrial Homeostasis During Infection: A Double-Edged Sword

Wang, Sutian; Zhang, Kunli; Yao, Yuchang; Li, Jianhao

doi:10.3389/fcell.2021.738932

Cited by 14 publications

(11 citation statements)

References 86 publications

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“…Moreover, MiR-181b plays a protective role in KA-induced epileptic juvenile rats by attenuating autophagy and apoptosis ( Wang et al, 2019 ). Therefore, autophagy is a double-edged sword and may play different roles in different diseases and disease progress ( Wang et al, 2021 ). Our previous studies have also shown that the effect of autophagy on flap viability is controversial and needs further research ( Li et al, 2020 ; Zhang et al, 2020 ; Chen et al, 2021 ; Zhu et al, 2021 ; Lou et al, 2022 ).…”

Section: Introductionmentioning

confidence: 99%

Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

et al. 2022

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The multiterritory perforator flap is one of the widest flap patterns used to repair tissue defects. However, flap necrosis of the distal part is still a challenging issue for plastic surgeons. Diallyl trisulfide (DATS) is an efficient ingredient extracted from garlic, exerting many important effects on different diseases. Our experiment aims to reveal whether DATS has a beneficial effect on the survival of perforator flaps and to explore its mechanism of action. The results showed that DATS enhanced angiogenesis and autophagy and reduced cell apoptosis and oxidative stress, thereby improving the survival rate of skin flaps. After co-administration with autophagy inhibitor 3-methyladenine (3MA), perforator flap survival was further improved. Mechanistically, we showed that PI3K/Akt and AMPK-HIF-1α signaling pathways in flap were activated under DATS treatment. All in all, DATS promoted the survival of multiterritory perforator flaps via the synergistic regulation of PI3K/Akt and AMPK-HIF-1α signaling pathways, and inhibition of DATS-induced autophagy further improves flap survival.

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Section: Introductionmentioning

confidence: 99%

Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

et al. 2022

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“…Interestingly, mitochondria have been reported to be important direct targets of Ca 2+ ; therefore, we considered whether HAP‐released Ca 2+ might help maintain mitochondrial homeostasis. Previous results have shown that mitochondrial dysfunction is closely related to cell viability 33 . The mitochondrial permeability‐transition pore (mPTP) is composed of a group of protein complexes that exist between the inner and outer membranes of mitochondria and help maintain the mitochondrial‐membrane potential (MMP) and ion balance between the inside and outside of cells 34 .…”

Section: Resultsmentioning

confidence: 99%

Curcumin/L‐OHP co‐loaded HAP for cGAS‐STING pathway activation to enhance the natural immune response in colorectal cancer

Xiao,

Guo,

Wang

et al. 2023

Bioengineering & Transla Med

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Insufficient immune cell infiltration into the tumor microenvironment (TME) greatly compromises the clinical application of immune‐checkpoint inhibitors (ICIs)‐based immunotherapy. Recent findings have shown that activation of the cyclic GMP‐AMP synthase‐stimulator of interferon genes (cGAS‐STING) pathway can enhance natural immunity and increase lymphocyte infiltration into the TME, which presents a promising strategy for cancer immunotherapy. In this study, we constructed hydroxyapatite nanoparticles co‐loaded with curcumin and L‐oxaliplatin (Cur/L‐OHP@HAP NPs). We analyzed the particle‐size distribution, zeta potential, spectral characteristics (Fourier‐transform infrared spectroscopy, X‐ray photoelectron spectroscopy, ultraviolet–visible spectroscopy), and drug‐release properties of the Cur/L‐OHP@HAP NPs. The cellular uptake of the Cur/L‐OHP@HAP NPs detected by flow cytometry and confocal laser‐scanning microscopy. We comprehensively evaluated the anti‐tumor properties and immune‐activating effects of the NPs, both in vitro and in vivo. Physicochemical characterizations demonstrated that the Cur/L‐OHP@HAP NPs were successfully synthesized and were capable of pH‐dependent drug release. Notably, the Cur/L‐OHP@HAP NPs efficiently entered cancer cells, after which the released L‐OHP induced nuclear DNA (nDNA) damage to some extent. HAP promoted the release of intracellular Ca2+ stores in cancer cells, and curcumin inhibited Ca2+ efflux, resulting in intracellular Ca2+ overload and the release of mitochondrial DNA (mtDNA). Damage to both nDNA and mtDNA greatly stimulated the cGAS‐STING pathway, thereby activating natural immunity, accompanied by immune cell recruitment to the TME. In summary, the Cur/L‐OHP@HAP NPs show good prospects for improving cancer immunotherapy.

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“…Autophagy, as a fundamental cellular degradation mechanism in eukaryotes, is equally important in innate immune defence and pathogenic microbe clearance [ 86 , 87 ]. Bacteria induce autophagy by stimulating innate immune receptors such as TLRs.…”

Section: E Faecalis -Modulated Host Cell Responsesmentioning

confidence: 99%

Role of Enterococcus faecalis in refractory apical periodontitis: from pathogenicity to host cell response

Deng

Lin

Liu

et al. 2023

Journal of Oral Microbiology

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Background: Refractory apical periodontitis (RAP) is an oral infectious disease characterised by persistent inflammation, progressive alveolar bone destruction, and delayed bone healing. RAP has received increasing attention, because it cannot be cured after repeated root canal therapies. The aetiology of RAP is related to the complex interplay between the pathogen and its host. However, the exact pathogenesis of RAP remains unclarified and includes several factors, such as microorganism immunogenicity, host immunity and inflammation, and tissue destruction and repair. Enterococcus faecalis is the dominant pathogen involved in RAP, and has evolved multiple strategies to ensure survival, which cause persistent intraradicular and extraradicular infections. Objective: To review the crucial role of E. faecalis in the pathogenesis of RAP, and open new avenues for prevention and treatment of RAP. Methods: The PubMed and Web of Science databases were searched for pertinent publications, employing the search terms “Enterococcus faecalis”, “refractory apical periodontitis”, “persistent periapical periodontitis”, “pathogenicity”, “virulence”, “biofilm formation”, “dentine tubule”, “immune cell”, “macrophage”, and “osteoblast”. Results and Conclusion: Besides its high pathogenicity due to various virulence mechanisms, E. faecalis modulates the macrophage and osteoblast responses, including regulated cell death, cell polarisation, cell differentiation, and inflammatory response. An in-depth understanding of the multifaceted host cell responses modulated by E. faecalis will help to design potential future therapeutic strategies and overcome the challenges of sustained infection and delayed tissue healing in RAP.

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Autophagy and Mitochondrial Homeostasis During Infection: A Double-Edged Sword

Cited by 14 publications

References 86 publications

Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

Diallyl Trisulfide Enhances the Survival of Multiterritory Perforator Skin Flaps

Curcumin/L‐OHP co‐loaded HAP for cGAS‐STING pathway activation to enhance the natural immune response in colorectal cancer

Role of Enterococcus faecalis in refractory apical periodontitis: from pathogenicity to host cell response

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