About this Research Topic
This Research Topic is part of the DAMPs across the tree of life series:
Volume 1 - Plants
Volume 2 - Regulated Cell Death and Immune Responses
All organisms on the planet use Damage Associated Molecular Patterns (DAMPs) to signal that injury has occurred, in order to initiate repair, remodeling, and immunity. It suggests that DAMPs and DAMPs-initiated signaling systems might be the most primordial form of innate immunity and tissue repair systems in living organisms before sophisticated immune systems evolved. Therefore, studying DAMPs is relevant for various fields, including agriculture, insect control, cancer, wound healing, pregnancy, transplantation, and various inflammatory disorders.
There is growing evidence for a pathogenetic role of DAMPs in many human diseases including autoimmune and allergic diseases; polytrauma; solid organ injuries; atherosclerosis and cerebro-cardiovascular diseases; infectious disorders; metabolic and neurodegenerative diseases; and cancer.
These molecules are beginning to shape modern medicine in their use as diagnostics, prognostics, therapeutics, and vaccines. The etiopathogenetic matrix, common to all DAMP-promoted human diseases, can be seen in the sequence:1) there is an acute or chronic organ injury 2) regulated cell death is engaged 3) DAMPs are emitted 4) pathological innate/adaptive immune responses are induced. These processes can lead to:
(1) acute overshooting necroinflammation in terms of nonresolving hyper-inflammation leading to acute organ failure such as seen in systemic inflammatory response syndrome (SIRS);
(2) chronic systemic nonresolving inflammation associated with fibrogenesis (such as seen in atherosclerosis);
(3) chronic organ-specific nonresolving inflammation transitioning to progressive fibrosis leading to chronic organ failure (such as seen in renal fibrosis, liver cirrhosis, or chronic obstructive pulmonary disease).
Recent notions on “DAMPome”-mediated disorders suggest that inflammatory diseases are usually not only caused by injury-induced emission of “promoting DAMPs” but also by an insufficient generation of “suppressing DAMPs” (“SAMPs”) such as specialized pro-resolving mediators (SPMs) and Annexin A1. This imbalance in the generation of these two categories of molecules which – when balanced under homeostatic conditions – result in post-injury restitutio ad integrum, can be considered the fundamental disease-causing momentum.
In this Volume addressing DAMPs in Human Diseases, we welcome authors to submit Original Research and Review Articles focusing on, but not limited to, the following subtopics, related to either human diseases or experimental models of human diseases:
1. DAMPs and SAMPs as diagnostic and prognostic biomarkers
2. DAMPs as therapeutic targets (e.g., in hyperinflammatory/ chronic inflammatory diseases)
3. SAMPs as therapeutics (e.g., in chronic inflammatory diseases)
4. Pathogenetic role of DAMPs and SAMPs in experimental models
Volume 1 - Plants
Volume 2 - Regulated Cell Death and Immune Responses
All organisms on the planet use Damage Associated Molecular Patterns (DAMPs) to signal that injury has occurred, in order to initiate repair, remodeling, and immunity. It suggests that DAMPs and DAMPs-initiated signaling systems might be the most primordial form of innate immunity and tissue repair systems in living organisms before sophisticated immune systems evolved. Therefore, studying DAMPs is relevant for various fields, including agriculture, insect control, cancer, wound healing, pregnancy, transplantation, and various inflammatory disorders.
There is growing evidence for a pathogenetic role of DAMPs in many human diseases including autoimmune and allergic diseases; polytrauma; solid organ injuries; atherosclerosis and cerebro-cardiovascular diseases; infectious disorders; metabolic and neurodegenerative diseases; and cancer.
These molecules are beginning to shape modern medicine in their use as diagnostics, prognostics, therapeutics, and vaccines. The etiopathogenetic matrix, common to all DAMP-promoted human diseases, can be seen in the sequence:1) there is an acute or chronic organ injury 2) regulated cell death is engaged 3) DAMPs are emitted 4) pathological innate/adaptive immune responses are induced. These processes can lead to:
(1) acute overshooting necroinflammation in terms of nonresolving hyper-inflammation leading to acute organ failure such as seen in systemic inflammatory response syndrome (SIRS);
(2) chronic systemic nonresolving inflammation associated with fibrogenesis (such as seen in atherosclerosis);
(3) chronic organ-specific nonresolving inflammation transitioning to progressive fibrosis leading to chronic organ failure (such as seen in renal fibrosis, liver cirrhosis, or chronic obstructive pulmonary disease).
Recent notions on “DAMPome”-mediated disorders suggest that inflammatory diseases are usually not only caused by injury-induced emission of “promoting DAMPs” but also by an insufficient generation of “suppressing DAMPs” (“SAMPs”) such as specialized pro-resolving mediators (SPMs) and Annexin A1. This imbalance in the generation of these two categories of molecules which – when balanced under homeostatic conditions – result in post-injury restitutio ad integrum, can be considered the fundamental disease-causing momentum.
In this Volume addressing DAMPs in Human Diseases, we welcome authors to submit Original Research and Review Articles focusing on, but not limited to, the following subtopics, related to either human diseases or experimental models of human diseases:
1. DAMPs and SAMPs as diagnostic and prognostic biomarkers
2. DAMPs as therapeutic targets (e.g., in hyperinflammatory/ chronic inflammatory diseases)
3. SAMPs as therapeutics (e.g., in chronic inflammatory diseases)
4. Pathogenetic role of DAMPs and SAMPs in experimental models
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
