Endoplasmic Reticulum, Mitochondria, Lysosomes and Nucleus May Handle Calcium (Ca2+) in Pathophysiological Conditions: New Mechanisms and Molecular Targets
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Mitochondria".
Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 726
Special Issue Editor
Interests: intracellular Ca2+ stores; store-operated Ca2+ entry; ER-stress; lysosomal Ca2+ channels; neurodegeneration; stroke; ALS
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Recent findings have revealed that an alteration in calcium (Ca2+) homeostasis may take part in the pathogenesis of several neurodegenerative, cardiac, ocular, and renal diseases.
Many of these alterations are due to organellar Ca2+ dyshomeostasis. Importantly, Ca2+-storing organelles interact with each other at specialized domains containing specific ionic channels, Ca2+-dependent proteins, etc.
Besides the folding of newly synthesized proteins, the endoplasmic reticulum (ER) has an essential function in storing Ca2+ ions. It has been established that prolonged ER Ca2+ leakage results in cell death via ER stress. This occurs through the activation of specific intracellular pathways.
Furthermore, nuclear calcium concentration ([Ca2+]n) may also be controlled independently from cytosolic events by local machinery handling Ca2+. Such Ca2+ transfer reduces the abnormal elevation of [Ca2+]n, thus modulating specific transductional pathways and providing a protective mechanism against cell death. Interestingly, the perinuclear space is adjacent to the lumen of ER, thus allowing a direct exchange of ions and factors between the two organelles. The same occurs between lysosomes and ER, lysosomes and mitochondria, and ER and mitochondria. However, many of these mechanisms remain unknown.
This Special Issue will focus on the possible role of organellar Ca2+ dyshomeostasis due to the dysfunction in these coupling mechanisms among the organelles in order to shed light on new promising targets for preventing or, at least, delaying degeneration in Ca2+-dependent diseases.
Dr. Agnese Secondo
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. 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
- Ca2+-storing organelles
- lysosomes
- ER
- nucleus
- mitochondria
- Ca2+-dependent disease
