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Molecular Mechanisms of Endoplasmic Reticulum Stress and Protein Homeostasis in Diseases

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

Deadline for manuscript submissions: 31 January 2027 | Viewed by 92

Editor


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Guest Editor
Department of Pharmacy, University of Salerno, Via G. Paolo II, 84084 Fisciano, SA, Italy
Interests: oxidative stress; neurodegenerative diseases; misfolding protein; corrector; inflammation; ER stress; calcium homeostasis; proteostasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Maintaining protein homeostasis (proteostasis) is fundamental for cellular survival, and its disruption is a defining hallmark of numerous human pathologies. The endoplasmic reticulum (ER) serves as the primary hub for protein folding and quality control; however, physiological demands, environmental insults, or genetic mutations can overwhelm its capacity, triggering ER stress. To counteract this, cells activate the Unfolded Protein Response (UPR), an intricate adaptive network that modulates translation, transcription, and degradation pathways. While initially protective, chronic or unresolved UPR signaling transitions into a pathological driver, leading to cellular dysfunction, inflammation, and cell death.

This Special Issue aims to provide a comprehensive, holistic overview of the molecular mechanisms underlying ER stress and its profound impact on proteostasis in disease contexts. The scope of this collection spans from basic organelle biology to translational medicine, welcoming original research and comprehensive reviews that explore UPR signaling dynamics, protein quality control networks (including ER-associated degradation and ER-phagy), and the critical functional correlation between ER stress and mitochondrial dysfunction. By investigating these pathways across various disease models—such as neurodegeneration, diabetes, cardiovascular disorders, and cancer—this issue seeks to highlight novel therapeutic interventions, including chemical chaperones and small-molecule modulators, capable of restoring proteostatic balance.

We look forward to receiving your contributions.

Dr. Michela Pecoraro
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 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-anonymized 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 2400 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

  • endoplasmic reticulum stress
  • unfolded protein response (UPR)
  • protein homeostasis
  • mitochondria-ER crosstalk
  • ERAD
  • proteotoxicity
  • neurodegeneration
  • translational therapeutics

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Published Papers

This special issue is now open for submission.
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