Special Issue "Mitochondrial Permeability Transition"
Deadline for manuscript submissions: closed (30 November 2020).
Interests: mitochondria; calcium; channels; permeability transition; ATP synthase; cell death
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Special Issue in Cells: 10th Anniversary of Cells—Advances in Organelle Function
Interests: role of mitochondria in cell death; permeability transition pore; inorganic polyphosphate in mammalian cells; calcium signaling; energy metabolism
For mitochondria to fulfill their bioenergetic function, mitochondrial inner membrane permeability needs to be tightly regulated. According to the fourth postulate of the chemiosmotic hypothesis, the inner membrane is a “specialised coupling membrane which has a low permeability to protons and to anions and cations generally” (Mitchell, P. Chemiosmotic coupling in oxidative and photosynthetic phosphorylation, Glynn Research, Bodmin Cornwall, England 1966, reprinted in Biochim Biophys Acta 2011, 1807, 1507-1538). This allows harnessing of the proton gradient through ATP synthase, completing the final step of oxidative phosphorylation. The mitochondrial permeability transition (mPT) is a reversible permeability increase of the inner membrane that can be triggered by matrix Ca2+. Initially considered an in vitro artifact, today the mPT is considered to be a regulated process mediated by opening of a high-conductance channel, the permeability transition pore (PTP). The PTP is currently investigated both as a physiological process involved in modulation of mitochondrial function and as a central event leading to disruption of cellular energy metabolism and cell death. As a pathological event, the mPT has been implicated as a central cause of cell damage in many conditions, including stroke, heart ischemia-reperfusion injury, muscular dystrophies and neurodegenerative diseases. Recent breakthrough discoveries have been made that significantly advance our understanding of the mPT. At the same time, these discoveries led to increasing appreciation of the tremendous complexity of the mPT, to the generation of new exciting theories and to new challenges, which are the matter of a lively debate. This Special Issue will focus on current progress in understanding the molecular mechanisms and pathophysiological role of this multifaceted phenomenon. We hope that it will serve as a platform for the exchange of new ideas and that it will further stimulate the development of the field.
Prof. Paolo Bernardi
Dr. Evgeny V. Pavlov
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 papers will be 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 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 2000 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.
- permeability transition pore
- ATP synthase
- adenine nucleotide translocator
- cyclophilin D