Dermal defection and the degree of its loss determine the natural process of wound healing, which is the key reason leading to excess scar hyperplasia. The function of tri-dimensional structure in dermis acts as a template to regulate the properties of reparative cells. The template structure induces the reparative cells to grow into the structure which changes the skin mechanic status on wound area. Also, the component of extracellular matrix can affect behaviours of fibroblasts negatively or positively, for the reason that the structure of dermal tissue has a permissive effect on the dermal components in regulating behaviours of reparative cells. Therefore, the behaviors of cells depend on the structure of the template. The suitable tri-dimensional structure of dermis facilitates normal cell cycling. The more the structure of dermis closed to its physiological status, the better the biological behaviors of cells act. Moreover, the integrity as well as the continuity of dermal tissue is the prerequisite for serving as a template. The damage to the integrity and the continuity of dermal tissue may be one of the key reasons to lead abnormal tissue repair and scar formation. Thus, we hypothesize that the loss of dermal template may be one of the mechanism of abnormal scar formation and propose the theory of extracellular matrix framework deficiency or destruction.
Download full-text PDF |
Source |
---|
Wound Repair Regen
January 2025
Department of Burn, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Bacterial colonisation in hypertrophic scars (HSs) has been reported, yet the precise mechanism of their contribution to scar formation remains elusive. To address this, we examined HS and normal skin (NS) tissues through Gram staining and immunofluorescence. We co-cultured fibroblasts with heat-inactivated Staphylococcus aureus (S.
View Article and Find Full Text PDFIndian J Thorac Cardiovasc Surg
February 2025
Department of Cardiology, G.B. Pant Institute of Postgraduate Medical Education & Research and associated Maulana Azad Medical College, Room No. 133, First Floor, Academic Block, New Delhi, India.
Left ventricular (LV) pseudoaneurysm, a rare occurrence, develops when a ruptured ventricle is encapsulated by the pericardium or scar tissue. Unlike free intrapericardial rupture, which often results in cardiac tamponade and fatal outcome, there are instances where the cardiac rupture remains contained, forming a pseudoaneurysm and averting immediate tamponade. We describe a 43-year-old male who underwent successful surgical repair of LV rupture following inferior wall myocardial infarction that resulted in the formation of a large pseudoaneurysm.
View Article and Find Full Text PDFBurns Trauma
January 2025
Department of Surgery, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH, 45267, USA.
Background: Keloids are disfiguring, fibrotic scar-like lesions that are challenging to treat and commonly recur after therapy. A deeper understanding of the mechanisms driving keloid formation is necessary for the development of more effective therapies. Reduced vitamin D receptor (VDR) expression has been observed in keloids, implicating vitamin D signaling in keloid pathology.
View Article and Find Full Text PDFASN Neuro
January 2025
Department of Cell & Developmental Biology, SUNY Upstate Medical University, Syracuse, NY, USA.
Functional recovery following spinal cord injury will require the regeneration and repair of damaged neuronal pathways. It is well known that the tissue response to injury involves inflammation and the formation of a glial scar at the lesion site, which significantly impairs the capacity for neuronal regeneration and functional recovery. There are initial attempts by both supraspinal and intraspinal neurons to regenerate damaged axons, often influenced by the neighboring tissue pathology.
View Article and Find Full Text PDFIBRO Neurosci Rep
June 2025
Université de la Réunion, INSERM, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Saint-Pierre 97410, France.
It is well recognized that type II Diabetes (T2D) and overweight/obesity are established risk factors for stroke, worsening also their consequences. However, the underlying mechanisms by which these disorders aggravate outcomes are not yet clear limiting the therapeutic opportunities. To fill this gap, we characterized, for the first time, the effects of T2D and obesity on the brain repair mechanisms occurring 7 days after stroke, notably glial scarring.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!