Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Autophagy in Inflammation-Associated Damage and Diseases
share announcement

Autophagy in Inflammation-Associated Damage and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 15408

Special Issue Editors

Dr. Hui-Wen Chiu

E-Mail Website
Guest Editor
Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei 11031, Taiwan
Interests: cell death; inflammation; kidney diseases; toxicology; nanomedicine
Dr. Yu-Hsuan Lee

E-Mail Website
Guest Editor
Department of Cosmeceutics, China Medical University, Taichung 406040, Taiwan
Interests: toxicology; skin immunology; skin aging; nanotoxicology; liver disease

Special Issue Information

Dear Colleagues,

During the past decade, human genetic studies have increasingly pointed to the involvement of autophagy, particularly in neurodegenerative diseases, cancers, and inflammatory diseases. Several studies have indicated that autophagy plays multiple roles in inflammatory responses; for example, autophagy is extensively utilized in dendritic cells (DCs), and solving its mechanism of action has possible implications for understanding skin and lung inflammation, as well as asthma. In addition, autophagy may also be critical for the protection of kidneys from versatile inflammatory insults and may regulate metabolic pathways in many diseases. More recently, accumulated data have revealed that dysregulated autophagy is linked to exosome production and the inflammasome in several diseases. This Special Issue focuses on the molecular aspects, immunological features, diagnostic tools, methods of prevention, and treatment strategies in the regulation of inflammatory damage and diseases by autophagy. All basic studies and translational research, including original articles and reviews, will be considered.

Dr. Huiwen Chiu
Dr. Yu-Hsuan Lee
Guest Editors

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • autophagy
  • apoptosis
  • inflammation
  • inflammasome
  • oxidative stress
  • endoplasmic reticulum stress
  • fibrosis
  • cancer therapy
  • exosome

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

23 pages, 4523 KiB  
Article
Methamphetamine Dysregulates Macrophage Functions and Autophagy to Mediate HIV Neuropathogenesis
by John M. Barbaro, Simone Sidoli, Ana Maria Cuervo and Joan W. Berman
Biomedicines 2022, 10(6), 1257; https://doi.org/10.3390/biomedicines10061257 - 27 May 2022
Cited by 2 | Viewed by 2281
Abstract
HIV-neurocognitive impairment (HIV-NCI) can be a debilitating condition for people with HIV (PWH), despite the success of antiretroviral therapy (ART). Substance use disorder is often a comorbidity with HIV infection. The use of methamphetamine (meth) increases systemic inflammation and CNS damage in PWH. [...] Read more.
HIV-neurocognitive impairment (HIV-NCI) can be a debilitating condition for people with HIV (PWH), despite the success of antiretroviral therapy (ART). Substance use disorder is often a comorbidity with HIV infection. The use of methamphetamine (meth) increases systemic inflammation and CNS damage in PWH. Meth may also increase neuropathogenesis through the functional dysregulation of cells that harbor HIV. Perivascular macrophages are long-lived reservoirs for HIV in the CNS. The impaired clearance of extracellular debris and increased release of reactive oxygen species (ROS) by HIV-infected macrophages cause neurotoxicity. Macroautophagy is a vital intracellular pathway that can regulate, in part, these deleterious processes. We found in HIV-infected primary human macrophages that meth inhibits phagocytosis of aggregated amyloid-β, increases total ROS, and dysregulates autophagic processes. Treatment with widely prescribed ART drugs had minimal effects, although there may be an improvement in phagocytosis when co-administered with meth. Pharmacologically inhibited lysosomal degradation, but not induction of autophagy, further increased ROS in response to meth. Using mass spectrometry, we identified the differentially expressed proteins in meth-treated, HIV-infected macrophages that participate in phagocytosis, mitochondrial function, redox metabolism, and autophagy. Significantly altered proteins may be novel targets for interventional strategies that restore functional homeostasis in HIV-infected macrophages to improve neurocognition in people with HIV-NCI using meth. Full article
(This article belongs to the Special Issue Autophagy in Inflammation-Associated Damage and Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Research

18 pages, 1421 KiB  
Review
Autophagy: Guardian of Skin Barrier
by Hyun Jee Kim, Jisoo Park, Sun Kyeon Kim, Hyungsun Park, Jung Eun Kim and Seongju Lee
Biomedicines 2022, 10(8), 1817; https://doi.org/10.3390/biomedicines10081817 - 28 Jul 2022
Cited by 11 | Viewed by 5461
Abstract
Autophagy is a major degradation pathway that removes harmful intracellular substances to maintain homeostasis. Various stressors, such as starvation and oxidative stress, upregulate autophagy, and the dysregulation of autophagy is associated with various human diseases, including cancer and skin diseases. The skin is [...] Read more.
Autophagy is a major degradation pathway that removes harmful intracellular substances to maintain homeostasis. Various stressors, such as starvation and oxidative stress, upregulate autophagy, and the dysregulation of autophagy is associated with various human diseases, including cancer and skin diseases. The skin is the first defense barrier against external environmental hazards such as invading pathogens, ultraviolet rays, chemical toxins, and heat. Although the skin is exposed to various stressors that can activate autophagy, the roles of autophagy in the skin have not yet been fully elucidated. Accumulating evidence suggests that autophagy is closely associated with pathogenesis and the treatment of immune-related skin diseases. In this study, we review how autophagy interacts with skin cells, including keratinocytes and immune cells, enabling them to successfully perform their protective functions by eliminating pathogens and maintaining skin homeostasis. Furthermore, we discuss the implications of autophagy in immune-related skin diseases, such as alopecia areata, psoriasis, and atopic dermatitis, and suggest that a combination of autophagy modulators with conventional therapies may be a better strategy for the treatment of these diseases. Full article
(This article belongs to the Special Issue Autophagy in Inflammation-Associated Damage and Diseases)
►▼ Show Figures

Figure 1

17 pages, 8381 KiB  
Review
ER-phagy in the Occurrence and Development of Cancer
by Huimin Zhou, Kexin Wang, Mengyan Wang, Wenxia Zhao, Conghui Zhang, Meilian Cai, Yuhan Qiu, Tianshu Zhang, Rongguang Shao and Wuli Zhao
Biomedicines 2022, 10(3), 707; https://doi.org/10.3390/biomedicines10030707 - 18 Mar 2022
Cited by 6 | Viewed by 2593
Abstract
As an organelle, the endoplasmic reticulum (ER) is closely related to protein synthesis and modification. When physiological or pathological stimuli induce disorders of ER function, misfolded proteins trigger ER-phagy, which is beneficial for restoring cell homeostasis or promoting cell apoptosis. As a double-edged [...] Read more.
As an organelle, the endoplasmic reticulum (ER) is closely related to protein synthesis and modification. When physiological or pathological stimuli induce disorders of ER function, misfolded proteins trigger ER-phagy, which is beneficial for restoring cell homeostasis or promoting cell apoptosis. As a double-edged sword, ER-phagy actively participates in various stages of development and progression in tumor cells, regulating tumorigenesis and maintaining tumor cell homeostasis. Through the unfolded protein response (UPR), the B cell lymphoma 2 (BCL-2) protein family, the Caspase signaling pathway, and others, ER-phagy plays an initiating role in tumor occurrence, migration, stemness, and proliferation. At the same time, many vital proteins strongly associated with ER-phagy, such as family with sequence similarity 134 member B (FAM134B), translocation protein SEC62 (SEC62), and C/EBP-homologous protein (CHOP), can produce a marked effect in many complex environments, which ultimately lead to entirely different tumor fates. Our article comprehensively focused on introducing the relationship and interaction between ER-phagy and cancers, as well as their molecular mechanism and regulatory pathways. Via these analyses, we tried to clarify the possibility of ER-phagy as a potential target for cancer therapy and provide ideas for further research. Full article
(This article belongs to the Special Issue Autophagy in Inflammation-Associated Damage and Diseases)
►▼ Show Figures

Figure 1

19 pages, 2615 KiB  
Review
Klotho an Autophagy Stimulator as a Potential Therapeutic Target for Alzheimer’s Disease: A Review
by Tsz Yan Fung, Ashok Iyaswamy, Sravan G. Sreenivasmurthy, Senthilkumar Krishnamoorthi, Xin-Jie Guan, Zhou Zhu, Cheng-Fu Su, Jia Liu, Yuxuan Kan, Yuan Zhang, Hoi Leong Xavier Wong and Min Li
Biomedicines 2022, 10(3), 705; https://doi.org/10.3390/biomedicines10030705 - 18 Mar 2022
Cited by 14 | Viewed by 4255
Abstract
Alzheimer’s disease (AD) is an age-associated neurodegenerative disease; it is the most common cause of senile dementia. Klotho, a single-pass transmembrane protein primarily generated in the brain and kidney, is active in a variety of metabolic pathways involved in controlling neurodegeneration and ageing. [...] Read more.
Alzheimer’s disease (AD) is an age-associated neurodegenerative disease; it is the most common cause of senile dementia. Klotho, a single-pass transmembrane protein primarily generated in the brain and kidney, is active in a variety of metabolic pathways involved in controlling neurodegeneration and ageing. Recently, many studies have found that the upregulation of Klotho can improve pathological cognitive deficits in an AD mice model and have demonstrated that Klotho plays a role in the induction of autophagy, a major contributing factor for AD. Despite the close association between Klotho and neurodegenerative diseases, such as AD, the underlying mechanism by which Klotho contributes to AD remains poorly understood. In this paper, we will introduce the expression, location and structure of Klotho and its biological functions. Specifically, this review is devoted to the correlation of Klotho protein and the AD phenotype, such as the effect of Klotho in upregulating the amyloid-beta clearance and in inducing autophagy for the clearance of toxic proteins, by regulating the autophagy lysosomal pathway (ALP). In summary, the results of multiple studies point out that targeting Klotho would be a potential therapeutic strategy in AD treatment. Full article
(This article belongs to the Special Issue Autophagy in Inflammation-Associated Damage and Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop