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Autophagy and the Ubiquitin–Proteasome System: Regulators of Protein Homeostasis, Cell Death, and Disease Pathogenesis

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 1020

Special Issue Editor

Dr. Lei Dong

E-Mail Website
Guest Editor
State Key Laboratory of Molecular Medicine and Biological Diagnosis and Treatment (Ministry of Industry and Information Technology), School of Life Science, Beijing Institute of Technology, Beijing 100081, China
Interests: juvenile myelomonocytic leukemia; leukemogenesis; hematologic malignancies; targeted drug development; protein targets in cancer; phosphatases

Special Issue Information

Dear Colleagues,

The maintenance of protein homeostasis and organelle integrity and function is crucial for cellular homeostasis and cell viability. All intracellular proteins and most extracellular proteins are constantly being renewed, meaning they are continuously degraded and replaced by newly synthesized proteins. The degradation of intracellular proteins mainly occurs through two pathways: autophagy and the ubiquitin–proteasome system. Autophagy is the principal mechanism that mediates the delivery of various cellular cargoes to lysosomes for degradation and recycling, while the ubiquitin–proteasome system is a highly complex, ubiquitin-mediated protein degradation mechanism that is involved in the degradation of many intracellular proteins with high specificity.

At the molecular level, numerous studies have demonstrated various interactions between these two degradation pathways. Both autophagy and the ubiquitin–proteasome system can utilize ubiquitin as a common tag to degrade ubiquitinated substrates. Proteasomes tagged with ubiquitin can be cleared through autophagy, and autophagy-related proteins can also be degraded via the proteasome system. The two pathways regulate each other's activity, working together to maintain cellular homeostasis.

This Special Issue invites the submission of original research articles and reviews that elucidate the roles and interconnections of autophagy and the ubiquitin–proteasome system, uncovering the molecular mechanisms underlying the regulation of protein homeostasis and their roles in cell death and disease pathogenesis. We aim to advance our understanding of the pathology related to protein homeostasis and pave the way for innovative therapeutic strategies.

This Special Issue is co-led by Dr. Qin Xia from Beijing Institute of Technology, and Dr. Shuai Fan from Beijing Institute of Technology. We thank them for their contribution and involvement in proposing, promoting, and developing the Special Issue.

Dr. Lei Dong
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. Current Issues in Molecular Biology 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 2200 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
  • ubiquitin–proteasome system
  • protein homeostasis
  • autophagosome
  • cell death regulation
  • cancer
  • Alzheimer's disease

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Published Papers (2 papers)

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Research

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19 pages, 5478 KB  
Article
The Interaction of DMRTA2 with HSP90β Inhibits p53 Ubiquitination and Activates the p53 Pathway to Suppress the Malignant Progression of Non-Small-Cell Lung Cancer
by Shiyang Deng, Ling Li and Jiang Du
Curr. Issues Mol. Biol. 2025, 47(7), 497; https://doi.org/10.3390/cimb47070497 - 28 Jun 2025
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Abstract
Background: Lung cancer, predominantly NSCLC (80%), has a poor prognosis due to late diagnosis and limited treatment efficacy. DMRTA2 (DMRT5), a transcription factor linked to neural/germ cell development, is overexpressed in NSCLC per TCGA data, indicating its potential role in tumorigenesis and [...] Read more.
Background: Lung cancer, predominantly NSCLC (80%), has a poor prognosis due to late diagnosis and limited treatment efficacy. DMRTA2 (DMRT5), a transcription factor linked to neural/germ cell development, is overexpressed in NSCLC per TCGA data, indicating its potential role in tumorigenesis and as a therapeutic target. Methods: Conduct a comprehensive search of the relevant theoretical foundations. Based on this, differential expression analysis will be performed using the DESeq2 package in R on RNA-seq data from lung adenocarcinoma and lung squamous cell carcinoma in the TCGA database. The research will then employ various methods, including CRISPR genome editing, MTS assay, flow cytometry, Western blot, co-immunoprecipitation, immunofluorescence, and qRT-PCR. Results: Through experimental validation, we found that DMRTA2 mRNA is highly expressed in non-small-cell lung cancer (NSCLC) tissues and is negatively correlated with poor prognosis. DMRTA2 binds to HSP90β, inhibiting the interaction between HSP90β and p53, thereby suppressing p53 ubiquitination and nuclear export. This activates the p53 pathway, inhibiting the proliferation and invasion of lung cancer cells. Conclusions: In NSCLC, DMRTA2 acts as a context-dependent regulator, stabilizing wild-type p53 through competitive HSP90β binding to suppress tumors, while in p53-compromised cells, potentially engaging HSP90β or alternative pathways to promote malignancy. Its dual localization and transport interactions reveal multifunctional, stress-responsive roles beyond transcription. Full article
(This article belongs to the Special Issue Autophagy and the Ubiquitin–Proteasome System: Regulators of Protein Homeostasis, Cell Death, and Disease Pathogenesis)
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Review

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34 pages, 5331 KB  
Review
Inflammation, Apoptosis, and Fibrosis in Diabetic Nephropathy: Molecular Crosstalk in Proximal Tubular Epithelial Cells and Therapeutic Implications
by Xuanke Liu, Chunjiang Zhang, Yanjie Fu, Linlin Xie, Yijing Kong and Xiaoping Yang
Curr. Issues Mol. Biol. 2025, 47(11), 885; https://doi.org/10.3390/cimb47110885 (registering DOI) - 24 Oct 2025
Abstract
Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease worldwide, with proximal tubular epithelial cells (PTECs) playing a central role in its pathogenesis. Under hyperglycemic conditions, PTECs drive a pathological triad of inflammation, apoptosis, and fibrosis. Recent advances reveal that these [...] Read more.
Diabetic nephropathy (DN) remains the leading cause of end-stage renal disease worldwide, with proximal tubular epithelial cells (PTECs) playing a central role in its pathogenesis. Under hyperglycemic conditions, PTECs drive a pathological triad of inflammation, apoptosis, and fibrosis. Recent advances reveal that these processes interact synergistically to form a self-perpetuating vicious cycle, rather than operating in isolation. This review systematically elucidates the molecular mechanisms underlying this crosstalk in PTECs. Hyperglycemia induces reactive oxygen species (ROS) overproduction, advanced glycation end products (AGEs) accumulation, and endoplasmic reticulum stress (ERS), which collectively activate key inflammatory pathways (NF-κB, NLRP3, cGAS-STING). The resulting inflammatory milieu triggers apoptosis via death receptor and mitochondrial pathways, while apoptotic cells release damage-associated molecular patterns (DAMPs) that further amplify inflammation. Concurrently, fibrogenic signaling (TGF-β1/Smad, Hippo-YAP/TAZ) promotes epithelial–mesenchymal transition (EMT) and extracellular matrix (ECM) deposition. Crucially, the resulting fibrotic microenvironment reciprocally exacerbates inflammation and apoptosis through mechanical stress and hypoxia. Quantitative data from preclinical and clinical studies are integrated to underscore the magnitude of these effects. Current therapeutic strategies are evolving toward multi-target interventions against this pathological network. We contrast the paradigm of monotargeted agents (e.g., Finerenone, SGLT2 inhibitors), which offer high specificity, with that of multi-targeted natural product-based formulations (e.g., Huangkui capsule, Astragaloside IV), which provide synergistic multi-pathway modulation. Emerging approaches (metabolic reprogramming, epigenetic regulation, mechanobiological signaling) hold promise for reversing fibrosis. Future directions include leveraging single-cell technologies to decipher PTEC heterogeneity and developing kidney-targeted drug delivery systems. We conclude that disrupting the inflammation–apoptosis–fibrosis vicious cycle in PTECs is central to developing next-generation therapies for DN. Full article
(This article belongs to the Special Issue Autophagy and the Ubiquitin–Proteasome System: Regulators of Protein Homeostasis, Cell Death, and Disease Pathogenesis)
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