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Autophagy and Oxidative Stress

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 2463

Special Issue Editors

Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Interests: autophagy; mitochondria; post-translational modifications; oxidative stress; cancer therapy

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Guest Editor
Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou 510632, China
Interests: proteomics; dark protein; mitochondria; reactive oxygen species; post-translational modification

Special Issue Information

Dear Colleagues,

Autophagy is an evolutionarily conserved catabolic process used to recycle cytoplasmic material. This process is enabled through the formation of a double membrane vesicle called an autophagosome, which transports cellular material to lysosomes for degradation, and allows cells to maintain cellular homeostasis under basal conditions and ensure survival after exposure to stress factors. Recently, many selective autophagy types, including mitophagy, ER-phagy, and ribophagy, have been investigated and found to play important roles in the physiological functions. Oxidative stress is closely associated with autophagy that resulting from various exogenous and endogenous stimuli, such as DNA damage, and chemotherapeutic drugs. It is interesting to investigate how cells fine-tune the balance between homeostasis and stress and navigate the decision between survival and cell death. Therefore, efforts to modify autophagy and oxidative stress pathways to improve disease therapy are necessary, ; however, much remains to be understood about their regulators, their modifications, and some relavant relevant disease states (such as cancers). Targeting essential components of the autophagy machinery may be the leading therapeutical strategy for clinical treatment. Many small molecules, like hydroxychloroquine and rapamycin et al., and natural products (quercetin and liensinine, et al.) were proved to exhibit a significant therapeutic effect on diseases. It is interesting to understand the role of autophagy and oxidative stress regulators in diseases and mining effective drugs for clinical treatment. The topic of this special issue is cell biology, clinical advances in autophagy and oxidative stress, and new treatment strategies, including targeted therapies or immunotherapies. Studies using animal or cell culture models to investigate molecular mechanisms of autophagy or oxidative stress, new autophagy or oxdative stress inducer/inhibitor, as well as stratagies for the treatment of diseases related to autophagy and oxidative stress will be published. Special attention will be given to studies on molecular mechanisms, therapeutic targets and autophagy or oxdative stress inducer/inhibitor.

For this Special Issue, we invite authors to submit novel work or reviews establishing the importance of autophagy or oxidative stress in the cell biology or pathology of human diseases, including cancer. This Special Issue aims at shedding new light on how autophagy and oxidative stress lead to an increase in disease pathology. Moreover, it aims at highlighting the cross-talk between autophagy and oxidative stress responses in the context of human diseases and relevant biomarker discovery.

Dr. Yang Wang
Prof. Dr. Qing-Yu He
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • oxidative stress
  • human diseases
  • cancer
  • drug
  • biomarker
  • therapy
  • multi-omics

Published Papers (2 papers)

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Research

17 pages, 12312 KiB  
Article
miR-30a-3p Regulates Autophagy in the Involution of Mice Mammary Glands
by Lei Tian, Shancheng Guo, Zhiye Zhao, Yuxu Chen, Chunmei Wang, Qingzhang Li and Ye Li
Int. J. Mol. Sci. 2023, 24(18), 14352; https://doi.org/10.3390/ijms241814352 - 20 Sep 2023
Viewed by 811
Abstract
The mammary gland undergoes intensive remodeling during the lactation cycle, and the involution process of mammary gland contains extensive epithelial cells involved in the process of autophagy. Our studies of mice mammary glands suggest that miR-30a-3p expression was low during involution compared with [...] Read more.
The mammary gland undergoes intensive remodeling during the lactation cycle, and the involution process of mammary gland contains extensive epithelial cells involved in the process of autophagy. Our studies of mice mammary glands suggest that miR-30a-3p expression was low during involution compared with its high expression in the mammary glands of lactating mice. Then, we revealed that miR-30a-3p negatively regulated autophagy by autophagy related 12 (Atg12) in mouse mammary gland epithelial cells (MMECs). Restoring ATG12, knocking down autophagy related 5 (Atg5), starvation, and Rapamycin were used to further confirm this conclusion. Overexpression of miR-30a-3p inhibited autophagy and altered mammary structure in the involution of the mammary glands of mice, which was indicative of alteration in mammary remodeling. Taken together, these results elucidated the molecular mechanisms of miR-30a-3p as a key induction mediator of autophagy by targeting Atg12 within the transition period between lactation and involution in mammary glands. Full article
(This article belongs to the Special Issue Autophagy and Oxidative Stress)
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13 pages, 2575 KiB  
Communication
Notch1 Is Involved in Physiologic Cardiac Hypertrophy of Mice via the p38 Signaling Pathway after Voluntary Running
by Weiwei Zhang, Jiayi Liu, Zekang Wu, Guanwei Fan, Zhuo Yang and Chunhua Liu
Int. J. Mol. Sci. 2023, 24(4), 3212; https://doi.org/10.3390/ijms24043212 - 6 Feb 2023
Cited by 1 | Viewed by 1121
Abstract
Appropriate exercise such as voluntary wheel-running can induce physiological cardiac hypertrophy. Notch1 plays an important role in cardiac hypertrophy; however, the experimental results are inconsistent. In this experiment, we aimed to explore the role of Notch1 in physiological cardiac hypertrophy. Twenty-nine adult male [...] Read more.
Appropriate exercise such as voluntary wheel-running can induce physiological cardiac hypertrophy. Notch1 plays an important role in cardiac hypertrophy; however, the experimental results are inconsistent. In this experiment, we aimed to explore the role of Notch1 in physiological cardiac hypertrophy. Twenty-nine adult male mice were randomly divided into a Notch1 heterozygous deficient control (Notch1+/− CON) group, a Notch1 heterozygous deficient running (Notch1+/− RUN) group, a wild type control (WT CON) group, and a wild type running (WT RUN) group. Mice in the Notch1+/− RUN and WT RUN groups had access to voluntary wheel-running for two weeks. Next, the cardiac function of all of the mice was examined by echocardiography. The H&E staining, Masson trichrome staining, and a Western blot assay were carried out to analyze cardiac hypertrophy, cardiac fibrosis, and the expression of proteins relating to cardiac hypertrophy. After two-weeks of running, the Notch1 receptor expression was decreased in the hearts of the WT RUN group. The degree of cardiac hypertrophy in the Notch1+/− RUN mice was lower than that of their littermate control. Compared to the Notch1+/− CON group, Notch1 heterozygous deficiency could lead to a decrease in Beclin-1 expression and the ratio of LC3II/LC3I in the Notch1+/− RUN group. The results suggest that Notch1 heterozygous deficiency could partly dampen the induction of autophagy. Moreover, Notch1 deficiency may lead to the inactivation of p38 and the reduction of β-catenin expression in the Notch1+/− RUN group. In conclusion, Notch1 plays a critical role in physiologic cardiac hypertrophy through the p38 signaling pathway. Our results will help to understand the underlying mechanism of Notch1 on physiological cardiac hypertrophy. Full article
(This article belongs to the Special Issue Autophagy and Oxidative Stress)
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