Inflammation in Redox Modulation during Pathophysiology
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".
Deadline for manuscript submissions: closed (25 August 2023) | Viewed by 1777
Special Issue Editors
2. Co-Lead, NIHR Clinical Research Network Cardiovascular (CRN) North East and North Cumbria, Translational and Clinical Research Institute, Newcastle upon Tyne, UK
3. Deputy Lead, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, International Centre for Life, Central Parkway, Newcastle Upon Tyne NE1 3BZ, UK
Interests: telomere biology; cellular senescence; cardiovascular biology and medicine
2. Co-Lead, Raja Peary Mohan College Integrated Biological Research Facility (RIBRF), Central Research Facility, Raja Peary Mohan College, Uttarpara, Hooghly, West Bengal, India
Interests: cardiac function; heart failure; echocardiography; myocardial infarction; cardiovascular medicine; clinical cardiology; apoptosis; plasmid cloning; molecular biology; nanobiotechnology
Special Issue Information
Dear Colleagues,
Background
Cardiac inflammation is characterised by reduced functional capacity and a potentially important role for the immune system in the pathogenesis of heart failure. A chronic inflammatory response can lead to local and systemic deleterious tissue response; the maladaptive outcome being counterproductive to healing progresses the pathological response. Typically, inflamed myocardium shows extracellular matrix (ECM) remodelling and is associated with an elevated level of reactive species (reactive oxygen species (ROS)/reactive nitrogen species (RNS)). ROS molecules trigger oxidative stress in a feedback mechanism involving cell death biological processes.
Goal
The goal of this Special Issue is to generate an in-depth overview of inflammatory processes in the development and progression of HFpEF and HfrEF, and deliberate on the mechanistic understanding of adverse myocardial remodelling processes post-cardiac injury. Significant efforts have been made to understand the role of inflammation in acute and chronic heart failure. A holistic understanding of organ crosstalk or cellular crosstalk by inflammatory mediators might be instrumental in redox regulation towards scar formation by tissue fibrosis. In this collection, we aim to understand the molecular roles underlying cardiac-inflammation-mediated redox regulation. Further, understanding the role of inflammation in myocardial pathological remodelling is of particular interest. The pathology triggered by maladaptive remodelling might be of interest for understanding therapeutic interventions. Thus, research articles addressing the signalling mechanisms that lead to redox regulation due to inflammation during pathophysiology will provide important insights into understanding the plethora of pathological diversity and progression of the disease.
Scope and information for Authors
In this Research Topic, authors are encouraged to submit comprehensive reviews, original research articles, cellular-signalling-based studies and OMICS-based studies pertaining to redox regulation/inflammation, animal-model-based mechanistic understandings and clinical articles describing any novel role of inflammatory molecules during pathology. A range of article types will be accepted that address, but are not limited to, the following:
- Inflammatory processes in myocardial pathological remodelling;
- Clinic trials addressing cardiovascular (cardiac) inflammation;
- DAMPs in fibrosis and cell death processes;
- Mechanistic understanding of inter-organ crosstalk;
- Association of cytokines with heart failure with preserved (HFpEF) and reduced ejection (HfrEF) fraction;
- Cardiomyocyte–fibroblast–immune-cell axis and crosstalk leading to ECM-remodeling;
- Mechanistic insights of cardiac-inflammation-mediated ageing;
- Mechanisms of known therapeutic targets and discoveries of novel therapeutic interventions;
- Role of inflammatory mediators in redox modulation during myocardial pathology;
- Role of the adaptive and innate immune system in cardiac inflammation;
- COVID-19-related cardiac inflammation;
- Role of cell death mechanisms and senescence in remodelling.
Prof. Dr. Ioakim Spyridopoulos
Dr. Santanu Rana
Guest Editors
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
- cardiomyocyte
- fibroblast
- extracellular matrix
- heart failure
- cell death
- inflammation
- redox signalling
- antioxidants
- DAMPs
