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Cells
Special Issues
Exclusive Reviews on Autophagy: From Molecular Mechanisms to Therapeutic Frontiers
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Exclusive Reviews on Autophagy: From Molecular Mechanisms to Therapeutic Frontiers

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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2074

Special Issue Editors

Prof. Dr. Chengyu Liang

E-Mail Website
Guest Editor
Ellen and Ronald Caplan Cancer Center, The Wistar Institute, Philadelphia, PA 19104, USA
Interests: autophagy; DNA damage repair; membrane trafficking; cancer biology; virus-host interaction
Prof. Dr. Daolin Tang

E-Mail Website
Guest Editor
Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Interests: immunometabolism and sepsis; PAMPs and DAMPs in immunity; pancreatic cancer; regulated cell death (ferroptosis, pyroptosis, alkaliptosis) and autophagy

Special Issue Information

Dear Colleagues,

In celebration of the 15th anniversary of Cells, we are delighted to launch an exclusive review Special Issue dedicated to autophagy, which is a fundamental and evolutionarily conserved catabolic process that maintains cellular homeostasis by degrading superfluous or damaged proteins, organelles, and pathogens through lysosomal recycling. Autophagy serves as a critical adaptive mechanism, safeguarding cells against stress, infection, and metabolic imbalance, while its dysregulation underpins a broad spectrum of diseases, including cancer, neurodegenerative disorders, metabolic syndromes, and aging.

As one of the most dynamic and rapidly advancing fields in contemporary life sciences, autophagy research continues to unravel novel molecular players, regulatory networks, and pathophysiological implications. This Special Issue aims to compile a curated collection of high‑quality, authoritative review articles that synthesize the latest breakthroughs in the field.

By bringing together visionary perspectives from diverse research communities, this exclusive Special Issue will not only commemorate the journal’s 15‑year legacy, but also chart future directions for autophagy research, inspiring innovation and collaboration in the years to come.

Prof. Dr. Chengyu Liang
Prof. Dr. Daolin Tang
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 250 words) can be sent to the Editorial Office for assessment.

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

  • autophagy
  • macro-autophagy
  • micro-autophagy
  • lysosomal degradation
  • adaptation to stresses
  • physiological functions and pathological situations

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Review

26 pages, 1387 KB  
Review
SQSTM1/p62 at the Crossroads of Autophagy, Inflammation, and Lethal Infection
by Ruoxi Zhang, Rui Kang and Daolin Tang
Cells 2026, 15(7), 652; https://doi.org/10.3390/cells15070652 - 7 Apr 2026
Viewed by 866
Abstract
Sequestosome 1 (SQSTM1, also known as p62) has emerged as a multifunctional signaling adaptor that bridges autophagy, proteostasis, and inflammation. In this review, we discuss the molecular mechanisms by which SQSTM1 regulates selective autophagy and immune signaling pathways, and how its dynamic modulation [...] Read more.
Sequestosome 1 (SQSTM1, also known as p62) has emerged as a multifunctional signaling adaptor that bridges autophagy, proteostasis, and inflammation. In this review, we discuss the molecular mechanisms by which SQSTM1 regulates selective autophagy and immune signaling pathways, and how its dynamic modulation shapes host responses during sepsis. We highlight the tissue-specific roles of SQSTM1 in sepsis-associated injury across major organs—including the liver, kidney, heart, lung, brain, and skeletal muscle—and explore its function as a damage-associated molecular pattern (DAMP) in the extracellular milieu. Recent studies implicate extracellular SQSTM1 in metabolic reprogramming and pro-inflammatory cytokine production via INSR signaling, supporting its classification as a novel DAMP and potential therapeutic target. We conclude a stage- and compartment-specific model for SQSTM1 during sepsis: its transition from a protective intracellular autophagy mediator in the early stage to a pathological extracellular DAMP in late stage. Furthermore, we discuss the translational relevance of pharmacological agents that modulate SQSTM1 levels or activity to restore immune balance and organ homeostasis. A better understanding of SQSTM1’s dual roles in immune activation and resolution could open new avenues for precision therapies in sepsis. Full article
(This article belongs to the Special Issue Exclusive Reviews on Autophagy: From Molecular Mechanisms to Therapeutic Frontiers)
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22 pages, 1984 KB  
Review
VPS34 in Autophagy, Cancer, and Cancer Therapy
by Elisabetta Bartolini, Bassam Janji and Ruize Gao
Cells 2026, 15(7), 636; https://doi.org/10.3390/cells15070636 - 1 Apr 2026
Viewed by 832
Abstract
Autophagy is a fundamental lysosome-dependent degradation process that maintains cellular homeostasis in response to stress. VSP34 (Vacuolar Protein Sorting 34, PIK3C3) is the only class-III phosphatidylinositol 3-kinase and generates phosphatidylinositol 3-phosphate (PI3P) for auto-phagosome nucleation and maturation. Thus, it provides a critical adaptive [...] Read more.
Autophagy is a fundamental lysosome-dependent degradation process that maintains cellular homeostasis in response to stress. VSP34 (Vacuolar Protein Sorting 34, PIK3C3) is the only class-III phosphatidylinositol 3-kinase and generates phosphatidylinositol 3-phosphate (PI3P) for auto-phagosome nucleation and maturation. Thus, it provides a critical adaptive survival pathway for cells that are experiencing metabolic stress. The VPS34–autophagy axis plays dual roles in cancer, which depend on the context: it can restrain early tumorigenesis, but in established tumors, it can promote survival in conditions of hypoxia, nutrient deprivation, and therapeutic pressure. Moreover, VPS34 shapes the tumor microenvironment (TME) through its influence on both immune and cancer cells by modulating autophagy, cGAS-STING (cyclic GMP-AMP synthase Stimulator of Interferon Genes), and STAT1 pathways. VPS34 inhibition has been reported to induce an interferon response that increases CD8+ T and natural killer (NK) cell infiltration and converts cold tumors into hot ones. This behavior suggests that combining VPS34 inhibitors with cancer immunotherapies could be beneficial. In this review, we summarize the molecular functions and regulations of VPS34 in autophagy and discuss recent advances linking VPS34 to tumor and cancer immunotherapy. Full article
(This article belongs to the Special Issue Exclusive Reviews on Autophagy: From Molecular Mechanisms to Therapeutic Frontiers)
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