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Cell Organelle Stress Responses and Implications in Human Diseases
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Cell Organelle Stress Responses and Implications in Human Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 894

Special Issue Editor

Dr. Jaeseok Han

E-Mail Website
Guest Editor
Soonchunhyang Institute of Medi-Bio Science (SIMS), Soonchunhyang University, Cheonan 31151, Republic of Korea
Interests: mitochondrial stress; ER stress; integrated stress response; metabolic diseases; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cellular organelles are specialized structures within cells that perform distinct functions necessary for cell survival and homeostasis. Examples of these include the endoplasmic reticulum (ER), the mitochondria, the lysosomes, the Golgi apparatus, and the nucleus. Each organelle faces various stress conditions that can disrupt its normal function, leading to a cascade of cellular dysfunctions.

Organelle stress responses are adaptive mechanisms that cells employ to cope with and mitigate the detrimental effects of stress and are crucial to maintaining cellular homeostasis and preventing cell death. However, chronic or overwhelming stress can lead to pathological conditions and contribute to the development of various human diseases.

This Special Issue aims to explore the diverse mechanisms of organelle stress responses and their implications in various human diseases. By understanding how different organelles respond to stress and the pathological consequences of these responses, we can identify novel therapeutic targets and strategies to treat or prevent diseases associated with organelle dysfunction.

Dr. Jaeseok Han
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. 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

  • organelle stresses
  • mitochondria
  • ER
  • lysosome
  • human diseases

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Published Papers (2 papers)

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Research

11 pages, 1894 KiB  
Communication
StarD5 Plays a Critical Role in the Hepatocyte ER Stress Survival Response
by William M. Pandak, Genta Kakiyama and Daniel Rodriguez-Agudo
Int. J. Mol. Sci. 2025, 26(9), 4157; https://doi.org/10.3390/ijms26094157 - 27 Apr 2025
Viewed by 126
Abstract
The unfolded protein response (UPR) is a highly orchestrated survival response initiated in cells under endoplasmic reticulum (ER) stress. Steroidogenic acute regulatory-related lipid transfer domain 5 (StarD5) is an ER stress-responsive, cholesterol-binding protein under the regulation of IRE1. Based upon in vitro findings, [...] Read more.
The unfolded protein response (UPR) is a highly orchestrated survival response initiated in cells under endoplasmic reticulum (ER) stress. Steroidogenic acute regulatory-related lipid transfer domain 5 (StarD5) is an ER stress-responsive, cholesterol-binding protein under the regulation of IRE1. Based upon in vitro findings, StarD5 delivers a protective response by translocating ER cholesterol to the plasma membrane (PM) and accompanying protective changes in PM fluidity. The study aimed to determine if StarD5′s ability to provide in vitro hepatocyte protective responses is translatable to in vivo conditions. ER stress in mouse livers was induced by intraperitoneal injection of tunicamycin (Tm). Adenovirus was used to restore the expression of StarD5 in the livers of StarD5−/− mice. Immunoblotting, histological analysis, and lipid measurements were performed. Induction of ER stress led to increased expression of StarD5 and steatosis in the livers of wild-type (WT) mice, while in StarD5−/− mice, steatosis and apoptosis were more acute compared to WT mice, as evidenced by increased lipid accumulation and cleavage of PARP, respectively. Selectively restoring StarD5 expression to ER-stressed StarD5−/− mice blunted the effects of tunicamycin. StarD5 appears to play a critical role in the ER stress survival response through its ability to regulate intracellular cholesterol homeostasis. Full article
(This article belongs to the Special Issue Cell Organelle Stress Responses and Implications in Human Diseases)
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18 pages, 1202 KiB  
Article
Negative Alterations in the Respiratory Activity of Isolated Crude Heart Mitochondria Following In Vivo Isoproterenol Injection in Rats Are Not Observed in Heart Homogenate Suggesting That the Isolation Procedure Generates Experimental Artefacts
by Dairo Alonso Rendon
Int. J. Mol. Sci. 2025, 26(6), 2388; https://doi.org/10.3390/ijms26062388 - 7 Mar 2025
Viewed by 372
Abstract
Mitochondrial respiratory parameters (state 2 mitochondrial respiratory activity (state 2), state 3 mitochondrial respiratory activity (state 3), respiratory control (RC), mitochondrial ATP synthetic activity (MASA), and oxidative phosphorylation efficiency (ADP:O)) were assayed in heart homogenates (HHs) and in unwashed isolated mitochondria (isolated crude [...] Read more.
Mitochondrial respiratory parameters (state 2 mitochondrial respiratory activity (state 2), state 3 mitochondrial respiratory activity (state 3), respiratory control (RC), mitochondrial ATP synthetic activity (MASA), and oxidative phosphorylation efficiency (ADP:O)) were assayed in heart homogenates (HHs) and in unwashed isolated mitochondria (isolated crude heart mitochondria (CHMs)), using rats sacrificed 3, 6, 24, and 48 h after receiving a subcutaneous injection of (−)-isoproterenol (67 mg/kg body weight). With HHs, the following was observed: (a) a statistically significant activation of RC and MASA at 3 h and 6 h after drug infusion; at those times, state 2, state 3, and ADP:O were not different. (b) No studied (−)-isoproterenol mitochondrial parameters were statistically different at 24 h and 48 h after drug administration. So extrapolating, (−)-isoproterenol treatment does not negatively impact mitochondrial respiratory function in vivo; on the contrary, a better 3 h and 6 h (−)-isoproterenol mitochondrial energetic functional state was observed. With CHMs, the following was observed: (a) a statistically significant activation of RC and MASA at 3 h, but no longer at 6 h after drug infusion. (b) No studied mitochondrial parameters were statistically different at 24 h after (−)-isoproterenol treatment, but at 48 h, a statistical decrease took place in (−)-isoproterenol RC, so the mitochondrial isolation procedure (MIP) causes additional negative alterations to the mitochondrial samples; therefore, isoproterenol-induced negative alterations of mitochondrial respiratory parameters reported in the literature using isolated heart mitochondria (IHMs) are possibly an experimental artefact. Full article
(This article belongs to the Special Issue Cell Organelle Stress Responses and Implications in Human Diseases)
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