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Cells
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Pharmacological Modulation of Autophagy
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Pharmacological Modulation of Autophagy

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 5500

Special Issue Editor

Prof. Dr. George G. Chen

E-Mail Website
Guest Editor
1. Senior Research Fellow, Department of Otorhinolaryngology, Head and Neck Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong
2. Emeritus Professor, Department of Surgery, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong
Interests: apoptosis in cancer (hepatocellular carcinoma, lung cancer and thyroid cancer)

Special Issue Information

Dear Colleagues,

Autophagy, a cell defensive mechanism, enables cells to recycle and utilize damaged organelles or/and degraded macromolecules so that cells can adapt themselves to harsh conditions such as cellular stress or insufficient nutrients. Therefore, general speaking, autophagy is a cell survival strategy against different stressors. Increasing evidence has demonstrated that autophagy plays a crucial role in both physiological and pathological conditions. Dysregulation of autophagy contributes to a wide variety of human diseases from cardiovascular disorders to cancers. A number of molecules, agents or protocols have been developed to target or modulate the autophagy, which either promotes or inhibits this survival process to facilitate the treatment. This Special Issue will welcome original articles related to targeting or/and modulating autophagy to benefit the disease treatment.

Prof. Dr. George G. Chen
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • autophagosome
  • autophagy
  • cell death
  • degradation
  • homeostasis
  • modulators
  • re-cycling
  • stress
  • survival
  • treatment

Published Papers (2 papers)

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Research

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15 pages, 4868 KiB  
Article
Hydroxysafflor Yellow A Exerts Neuroprotective Effects via HIF-1α/BNIP3 Pathway to Activate Neuronal Autophagy after OGD/R
by Ruheng Wei, Lijuan Song, Zhuyue Miao, Kexin Liu, Guangyuan Han, Haifei Zhang, Dong Ma, Jianjun Huang, Hao Tian, Baoguo Xiao and Cungen Ma
Cells 2022, 11(23), 3726; https://doi.org/10.3390/cells11233726 - 22 Nov 2022
Cited by 4 | Viewed by 1348
Abstract
In the process of ischemic stroke (IS), cellular macroautophagy/autophagy and apoptosis play a vital role in neuroprotection against it. Therefore, regulating their balance is a potential therapeutic strategy. It has been proved that hydroxysafflor yellow A (HSYA) has anti-inflammatory and antioxidant effects, which [...] Read more.
In the process of ischemic stroke (IS), cellular macroautophagy/autophagy and apoptosis play a vital role in neuroprotection against it. Therefore, regulating their balance is a potential therapeutic strategy. It has been proved that hydroxysafflor yellow A (HSYA) has anti-inflammatory and antioxidant effects, which can both protect neurons. By exploring bioinformatics combined with network pharmacology, we found that HIF1A and CASP3, key factors regulating autophagy and apoptosis, may be important targets of HSYA for neuroprotection in an oxygen glucose deprivation and reperfusion (OGD/R) model. In this study, we explored a possible new mechanism of HSYA neuroprotection in the OGD/R model. The results showed that OGD/R increased the expression of HIF1A and CASP3 in SH-SY5Y cells and induced autophagy and apoptosis, while HSYA intervention further promoted the expression of HIF1A and inhibited the level of CASP3, accompanied by an increase in autophagy and a decrease in apoptosis in SH-SY5Y cells. The inhibition of HIF1A diminished the activation of autophagy induced with HSYA, while the inhibition of autophagy increased cell apoptosis and blocked the neuroprotective effect of HSYA, suggesting that the neuroprotective effect of HSYA should be mediated by activating the HIF1A/BNIP3 signaling pathway to induce autophagy. These results demonstrate that HSYA may be a promising agent for treating IS. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Autophagy)
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Review

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18 pages, 3389 KiB  
Review
Chaperone-Mediated Autophagy in Neurodegenerative Diseases: Molecular Mechanisms and Pharmacological Opportunities
by Yi-Ting Wang and Jia-Hong Lu
Cells 2022, 11(14), 2250; https://doi.org/10.3390/cells11142250 - 20 Jul 2022
Cited by 17 | Viewed by 3684
Abstract
Chaperone-mediated autophagy (CMA) is a protein degradation mechanism through lysosomes. By targeting the KFERQ motif of the substrate, CMA is responsible for the degradation of about 30% of cytosolic proteins, including a series of proteins associated with neurodegenerative diseases (NDs). The fact that [...] Read more.
Chaperone-mediated autophagy (CMA) is a protein degradation mechanism through lysosomes. By targeting the KFERQ motif of the substrate, CMA is responsible for the degradation of about 30% of cytosolic proteins, including a series of proteins associated with neurodegenerative diseases (NDs). The fact that decreased activity of CMA is observed in NDs, and ND-associated mutant proteins, including alpha-synuclein and Tau, directly impair CMA activity reveals a possible vicious cycle of CMA impairment and pathogenic protein accumulation in ND development. Given the intrinsic connection between CMA dysfunction and ND, enhancement of CMA has been regarded as a strategy to counteract ND. Indeed, genetic and pharmacological approaches to modulate CMA have been shown to promote the degradation of ND-associated proteins and alleviate ND phenotypes in multiple ND models. This review summarizes the current knowledge on the mechanism of CMA with a focus on its relationship with NDs and discusses the therapeutic potential of CMA modulation for ND. Full article
(This article belongs to the Special Issue Pharmacological Modulation of Autophagy)
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