Tissue Regeneration and Repair in Airway Diseases
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 1495
Special Issue Editor
Interests: the aim is to arouse particular interest and understanding for the "other" side of the inflammatory process, namely the active maintenance of differentiated cell and organ structures and the associ-ated functions as an active inhibition of inflammation, as this fundamental change in awareness should lead to new and more effective treatment options for numerous age-associated inflammato-ry diseases
Special Issue Information
Dear Colleagues,
Millions of people around the world, usually from middle age onwards, suffer from currently incurable and relentlessly progressive diseases deeply affecting the structure and function of the human body and its organs. Typically, the pathology of these diseases centers on chronic inflammation and cancer or a combination of both.
While in recent decades a broad interest has developed towards a comprehensive understanding of the complex and intertwined metabolism underlying the development and progression of cancer, this does not apply to chronic inflammatory diseases (CIDs), in spite of their enormous medical significance. In addition, research in the field of chronic inflammatory diseases has largely focused on the details of the undoubtedly important inflammatory process itself.
Lately, however, it is being increasingly recognized that the loss of structural integrity itself may cause inflammation, and that a continued loss of the structural integrity of organs, combined with a growing inability to maintain adequate structural repair, may act as an important cause for progressive chronic inflammation. Ensuring structural integrity closely relates to regenerative repair or primary wound healing, which controls structural and functional renewal. In contrast, secondary repair or scar formation, or, more generally, fibrosis, is unsuccessful in restoring the primary structure and function of an organ.
This is particularly relevant for the lungs, which have an elastic and permeable surface area roughly equivalent to the size of a tennis court to ensure functionally adequate gas exchange. With each breath, this vast surface area is stretched by muscle force and then contracted again only by the elastic structure of the lung membranes, leading to lifelong, inevitable exposure to various irritants, toxins, or infectious agents. Therefore, the progressive loss of surface and matrix integrity in structurally and functionally critical compartments, such as the bronchi, particularly the smaller bronchi, and the alveolar space has tremendous effects, acute inflammation being just the first result. Not surprisingly, acute pneumonia is the most common cause of death in aging individuals—regardless of what other disorder is simultaneously occurring in the body.
Chronic pulmonary inflammation is equally disastrous, but less apparent, as the body’s regenerative repair capacity can mask its effects on structure and function. With few exceptions, the combined pathology of structural disintegration and reduced repair capacity will thus usually become apparent only later in life. This is unfortunate, because this combined pathology will become progressive at that stage, as the body has no primary repair capacity anymore with which to withstand it. The result is both renewed inflammation and a different repair quality called secondary repair (i.e., scarring = fibrosis).
The aim of this Special Issue is to review our current understanding of structural integrity and regenerative repair capacity for chronic inflammatory processes in the lung, although our understanding of this topic is still in its early stages.
Prof. Dr. Rolf Ziesche
Guest Editor
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Keywords
- chronic inflammation
- structural integrity
- regenerative repair
- structural disintegration
- impact of aging on inflammation and repair
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