Cardioprotection and Mitochondrial Signaling: Insights from Molecular Mechanisms to Therapeutic Strategies
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 May 2025 | Viewed by 132
Special Issue Editor
Special Issue Information
Dear Colleagues,
Mitochondrial dysfunction is a key feature of ischemia/reperfusion damage, as well as heart failure, both the leading causes of death and disability worldwide. Therefore, cardioprotective strategies to prevent alterations of the function of these organelles are currently directed toward reducing the formation of reactive oxygen species, inhibiting the opening of the mitochondrial permeability transition pore, regulating kinase signaling and maintaining mitochondrial quality control.
This Special Issue will publish original articles focused on mitochondria as a therapeutic target and novel forms of cardioprotection with the potential to be translated to clinical settings for improving outcomes in AMI patients and preventing heart failure.
All submissions will be peer-reviewed, following the same evaluation criteria as individual IJMS submissions.
Dr. Cecilia Zazueta
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.
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Keywords
- cardioprotection
- mitochondrial signaling
- mitochondrial dysfunction
- heart failure
- ischemia/reperfusion
- mitochondria
- reactive oxygen species
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