scholarly journals Reviewing the Physiology of Cutaneous Wound Healing and Evaluating the Effect of Exercise on it: A Narrative Review Article

2021 ◽  
Vol 19 (3) ◽  
Author(s):  
Fatima Riyahi ◽  
Simin Riahy ◽  
Mitra Yousefpour

Context: The skin is the most important organ of the body, and maintaining its integrity is important for health. Severe skin damage is life-threatening, and wound healing restores its integrity. One of the main health problems is impaired cutaneous wound healing. According to the importance of wound healing and the fact that unrepaired skin decreases the quality of life, many studies have investigated the effect of some natural and chemical substances on the length and quality of wound healing to find beneficial interventions for rapid and economical treatment. Objectives: This review was conducted to describe the physiology of cutaneous wound healing and some positive and negative factors affecting it with a focus on exercise. Methods: An electronic search without any time limitation was performed on the PubMed, Google Scholar, and Web of Science databases. The keywords were ‘wound’, ‘healing’, and ‘exercise’. Finally, according to the similarities or differences between the results and the relationship with the subject, 53 papers were selected and reviewed. Results: Wound healing is a complex physiological process with four overlapping processes. It seems that disturbance in the inflammatory phase of wound healing is the main factor in the impairment of healing. Traditionally, many chemical and herbal medicines and compounds have been used to speed up wound recovery due to their anti-inflammatory and antioxidative properties. Many studies have evaluated the effect of exercise, as complementary medicine, on wound healing, and they have examined the effect of different protocols of exercise on the speed of wound healing. According to the results of these studies, aerobic exercise, due to its anti-inflammatory and antioxidative effects, is a beneficial method in shortening the length of healing, especially in aged, obese, and diabetic individuals. Conclusions: Exercise as a low-cost intervention is a good strategy in the treatment of impaired and chronic wounds.

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Keizo Kohno ◽  
Satomi Koya-Miyata ◽  
Akira Harashima ◽  
Takahiko Tsukuda ◽  
Masataka Katakami ◽  
...  

Abstract Background NK-4 has been used to promote wound healing since the early-1950s; however, the mechanism of action of NK-4 is unknown. In this study, we examined whether NK-4 exerts a regulatory effect on macrophages, which play multiple roles during wound healing from the initial inflammatory phase until the tissue regeneration phase. Results NK-4 treatment of THP-1 macrophages induced morphological features characteristic of classically-activated M1 macrophages, an inflammatory cytokine profile, and increased expression of the M1 macrophage-associated molecules CD38 and CD86. Interestingly, NK-4 augmented TNF-α production by THP-1 macrophages in combination with LPS, Pam3CSK4, or poly(I:C). Furthermore, NK-4 treatment enhanced THP-1 macrophage phagocytosis of latex beads. These results indicate that NK-4 drives macrophage polarization toward an inflammatory M1-like phenotype with increased phagocytic activity. Efferocytosis is a crucial event for resolution of the inflammatory phase in wound healing. NK-4-treated THP-1 macrophages co-cultured with apoptotic Jurkat E6.1 (Apo-J) cells switched from an M1-like phenotype to an M2-like phenotype, as seen in the inverted ratio of TNF-α to IL-10 produced in response to LPS. We identified two separate mechanisms that are involved in this phenotypic switch. First, recognition of phosphatidylserine molecules on Apo-J cells by THP-1 macrophages downregulates TNF-α production. Second, phagocytosis of Apo-J cells by THP-1 macrophages and activation of PI3K/Akt signaling pathway upregulates IL-10 production. Conclusion It is postulated that the phenotypic switch from a proinflammatory M1-like phenotype to an anti-inflammatory M2-like phenotype is dysregulated due to impaired efferocytosis of apoptotic neutrophils at the wound site. Our results demonstrate that NK-4 improves phagocytosis of apoptotic cells, suggesting its potential as a therapeutic strategy to resolve sustained inflammation in chronic wounds.


Author(s):  
Ghazal Shabestani Monfared ◽  
Peter Ertl ◽  
Mario Rothbauer

Cutaneous wound healing is a complex multi-stage process involving direct and indirect cell communication events with the aim of efficiently restoring the barrier function of the skin. One key aspect in cutaneous wound healing is associated with cell movement and migration into the physically, chemically and biologically injured area resulting in wound closure. Understanding the conditions under which cell migration is impaired and elucidating the cellular and molecular mechanisms that improve healing dynamics is therefore crucial in devising novel therapeutic strategies to elevate patient suffering, reduce scaring and eliminate chronic wounds. Following the global trend towards automation, miniaturization and integration of cell-based assays into microphysiological systems, conventional wound healing assays such as the scratch assay or cell exclusion assay have recently been translated and improved using microfluidics and lab-on-a-chip technologies. These miniaturized cell analysis systems allow precise spatial and temporal control over a range of dynamic microenvironmental factors including shear stress, biochemical and oxygen gradients to create more reliable in vitro models that resemble the in vivo microenvironment of a wound more closely on a molecular, cellular, and tissue level. The current review provides (a) an overview on the main molecular and cellular processes that take place during wound healing, (b) a brief introduction into conventional in vitro wound healing assays, and (c) a perspective on future cutaneous and vascular wound healing research using microfluidic technology.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Na-Young Park ◽  
Giuseppe Valacchi ◽  
Yunsook Lim

Inflammatory response is considered the most important period that regulates the entire healing process. Conjugated linoleic acid (CLA), a class of linoleic acid positional and geometric isomers, is well known for its antioxidant and anti-inflammatory properties. We hypothesized that dietary CLA supplementation accelerates cutaneous wound healing by regulating antioxidant and anti-inflammatory functions. To investigate wound closure rates and inflammatory responses, we used a full-thickness excisional wound model after 2-week treatments with control, 0.5%, or 1% CLA-supplemented diet. Mice fed dietary CLA supplementation had reduced levels of oxidative stress and inflammatory markers. Moreover, the wound closure rate was improved significantly in mice fed a 1% CLA-supplemented diet during early stage of wound healing (inflammatory stage). We conclude that dietary CLA supplementation enhances the early stage of cutaneous wound healing as a result of modulating oxidative stress and inflammatory responses.


2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Myungsuk Kim ◽  
Hee Ju Lee ◽  
Ahmad Randy ◽  
Ji Ho Yun ◽  
Sang-Rok Oh ◽  
...  

2014 ◽  
Vol 20 (2) ◽  
pp. 322-330 ◽  
Author(s):  
Vinay Kant ◽  
Anu Gopal ◽  
Nitya N. Pathak ◽  
Pawan Kumar ◽  
Surendra K. Tandan ◽  
...  

2006 ◽  
Vol 96 (6) ◽  
pp. 1069-1077 ◽  
Author(s):  
Adriana P. Nascimento ◽  
Andréa M. A. Costa

Prolonged wound healing is a complication that contributes to morbidity and mortality. Overweight people regularly undergo surgery and trauma, and often develop chronic wounds, but the effects of the adipose tissue excess on cutaneous wound healing are not well understood. This study tested the hypothesis that overweight induced by a high-fat diet impairs rat cutaneous wound healing. Male Wistar rats were fed with either a high-fat or a standard (control) diet. After 15 weeks, an excisional lesion was done and the animals were killed 21 d later. Wound contraction and re-epithelialization, blood pressure, glucose and retroperitoneal fat were evaluated. After killing, lesion and adjacent normal skin were formol-fixed and paraffin-embedded. Inflammatory infiltrate, myofibroblasts, collagen fibres and cellular proliferation were analysed and blood vessels were evaluated using stereological methods. There was no difference in blood pressure and glucose, but retroperitoneal fat increased in the high-fat diet group. Animals fed with the high-fat diet presented delayed wound contraction and re-epithelialization. It was found that 21 d after wounding, overweight induced by a high-fat diet increased the inflammatory infiltrate and delayed myofibroblastic differentiation, collagen deposition, epithelial and connective tissue cell proliferation, and angiogenesis. These findings support the hypothesis that a high-fat diet exerts negative effects on rat cutaneous wound healing, due mainly to the prolongation of the inflammatory phase.


2008 ◽  
Vol 34 (2) ◽  
pp. 162-184 ◽  
Author(s):  
Sashwati Roy ◽  
Savita Khanna ◽  
Cameron Rink ◽  
Sabyasachi Biswas ◽  
Chandan K. Sen

This work represents a maiden effort to systematically screen the transcriptome of the healing wound-edge tissue temporally using high-density GeneChips. Changes during the acute inflammatory phase of murine excisional wounds were characterized histologically. Sets of genes that significantly changed in expression during healing could be segregated into the following five sets: up-early (6–24 h; cytokine-cytokine receptor interaction pathway), up-intermediary (12–96 h; leukocyte-endothelial interaction pathway), up-late (48–96 h; cell-cycle pathway), down-early (6–12 h; purine metabolism) and down-intermediary (12–96 h; oxidative phosphorylation pathway). Results from microarray and real-time PCR analyses were consistent. Results listing all genes that were significantly changed at any specific time point were further mined for cell-type (neutrophils, macrophages, endothelial, fibroblasts, and pluripotent stem cells) specificity. Candidate genes were also clustered on the basis of their functional annotation, linking them to inflammation, angiogenesis, reactive oxygen species (ROS), or extracellular matrix (ECM) categories. Rapid induction of genes encoding NADPH oxidase subunits and downregulation of catalase in response to wounding is consistent with the fact that low levels of endogenous H2O2is required for wound healing. Angiogenic genes, previously not connected to cutaneous wound healing, that were induced in the healing wound-edge included adiponectin, epiregulin, angiomotin, Nogo, and VEGF-B. This study provides a digested database that may serve as a valuable reference tool to develop novel hypotheses aiming to elucidate the biology of cutaneous wound healing comprehensively.


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