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Responding to stress: cellular and molecular mechanisms

Guest Editors:
Francesco Cappello: University of Palermo, Italy
Ryo Higuchi-Sanabria: University of Southern California, United States

Submission Status: Open   |   Submission Deadline: 1 July 2024

Cells are continuously exposed to environmental and/or intracellular stressors and need to limit the damage and potentially harmful effects caused by these stresses. BMC Molecular and Cell Biology invites submissions investigating the numerous cellular and molecular processes that cells used to defend against and respond to stressors. 

Responding to stress: cellular and molecular mechanisms

Meet the Guest Editors

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Francesco Cappello: University of Palermo, Italy

Full Professor, Human Anatomy, Histology & Embryology, University of Palermo (UniPA), Palermo, Italy - Vice-Rector for Student Life (UniPA) - Rector Delegate for Sicilian Biomedical District (UniPA) - Chief of the Center for the Enhancement of the Corpse Donated to Science (UniPA) - President (Honorific), Italian Society of Experimental Biology (SIBS), Italy - Scientific Director (Honorific), Euro-Mediterranean Institute of Science and Technology, Palermo, Italy - Associate Member (Honorific), Graduate School of Biomedical Sciences, UTMB, Galveston (TX), USA - Adjunct Professor (Honorific), Department of Biology, Temple University, Philadelphia (PA), USA - Senior Fellow (Honorific), Cell Stress Society International, USA

Ryo Higuchi-Sanabria: University of Southern California, United States

Ryo Sanabria’s experience differs considerably from that of the typical researcher – they come from a restaurant and retail management background for the first 10+ years of their professional life. As someone from a disadvantaged background, they hold immense value in promoting diversity and equity initiatives and prioritize mentorship and education of trainees. Scientifically, the Sanabria lab investigates how stress impacts the aging process. Specifically, they study how cellular stress responses of the actin cytoskeleton, mitochondria, and endoplasmic reticulum decline during aging and how improving the function of these stress responses can be utilized to combat aging and age-related disease. Putting the actin cytoskeleton at the center of their studies, they focus on actin-organelle interactions under cellular and organismal stress conditions.

About the collection

From the origin of life on earth, cells are continuously exposed to environmental and/or intracellular stressors, and in response to them, cells need to equip themselves with anti-stress mechanisms, e.g., activating protective pathways such as the heat-shock or DNA damage response, to defend and recover themselves. Many stress response pathways are highly conserved, from single-cell organisms to higher-order animals. Protective programs aim to keep the cell alive; however, if these fail or the stress continues, cells may ultimately initiate more destructive stress pathways resulting in cell death. For example, during aging, cellular stress responses decline in function, which results in several of the physiological consequences of aging. Increasingly the importance of cellular stress response and immune system activation is becoming clear, and aberrant stress response pathways are thought to play pivotal roles in a variety of non-communicable diseases ranging from neurodegenerative diseases to cancer to diabetes. Understanding the molecular and cellular mechanisms of these multi-component stress response pathways, their crosstalk, and their role in disease will aid the development of therapeutics for these diseases. As such, BMC Molecular and Cell Biology invites submissions on this topic, including but not limited to the following:

● Detection of stressors and downstream signaling pathways, such as the PIKK kinase signaling pathways
● Interplay and crosstalk between protective and destructive stress responses
● Mechanistic insight into the activation of the heat-shock pathways
● Activation of cell death pathways following stress response, including apoptosis, necrosis, cell-stress-induced autophagic death, pyroptosis, ferroptosis, and other cell death pathways
● Insight into the role of aberrant stress response pathways in disease, e.g., the unfolded protein response pathways in neurodegenerative diseases
● Molecular and cellular mechanisms of responding to DNA damage
● Interaction of stress response pathways and initiating innate immune responses during infection
● Molecular mechanisms of the oxidative stress response pathways
● Stress response pathways in bacteria and archaea
● Animal models of stress responses and preclinical disease models
● Role of stress responses in aging
● New insights on the chaperone system, chaperonopathies, and chaperonotherapies

Image credit: Andrii Yalanskyi /

  1. In recent years, the role of autophagy has been highlighted in the pathogenesis of diabetes and inflammatory lung diseases. In this study, using a diabetic model of mice, we investigated the expression of auto...

    Authors: Jafar Rezaie, Mojtaba Jahanghiri, Reza Mosaddeghi- Heris, Sina Hassannezhad, Nima Abdyazdani, Afshin Rahbarghazi and Mahdi Ahmadi
    Citation: BMC Molecular and Cell Biology 2024 25:7

Submission Guidelines

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This Collection welcomes submission of original Research Articles. Should you wish to submit a different article type, please read our submission guidelines to confirm that type is accepted by the journal. Articles for this Collection should be submitted via our submission system, Snapp. During the submission process you will be asked whether you are submitting to a Collection, please select "Responding to stress: cellular and molecular mechanisms" from the dropdown menu.

Articles will undergo the journal’s standard peer-review process and are subject to all of the journal’s standard policies. Articles will be added to the Collection as they are published.

The Guest Editors have no competing interests with the submissions which they handle through the peer review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests.