Association of plasminogen activator inhibitor‐1 and vitamin D receptor expression with the risk of keloid disease in a Chinese population

Ji, Jianfeng; Xiang, Tie; Zhou, Changkai; Pan, Xuanliang; Yao, Jing

doi:10.1016/j.kjms.2016.10.013

Cited by 14 publications

(12 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…65 The scar-limiting activity of vitamin D is further supported by the analysis by Gong et al of 236 keloid patients and 219 age-and sex-matched healthy controls that showed keloid patient peripheral blood lymphocytes had significantly lower levels of vitamin D receptor (VDR) mRNA. 66 VDR is a member of the steroid nuclear receptor superfamily that, when bound to the active form of vitamin D, translocates from the cytoplasm to the nucleus and then binds to vitamin D-response elements on the DNA, resulting in the inflammation-and fibrosis-inhibiting activities of vitamin D. 67,68 Similarly, Hahn et al found that excised keloid lesions (n = 24) had overall lower VDR protein levels than skin samples from non-keloid surgical patients (n = 24). Moreover, the epidermis of the keloid samples exhibited significantly less nuclear localization of VDR than the normal samples.…”

Section: Vitamin Dmentioning

confidence: 99%

Systemic factors that shape cutaneous pathological scarring

Huang

Ogawa

2020

FASEB j.

View full text Add to dashboard Cite

Cutaneous pathological scars are fibrotic lesions that grow continuously, invade the adjacent skin, and are erythematous, itchy, and painful. Their etiology remains unclear but may involve genetic, local mechanical, and systemic factors. Here, we will summarize the main systemic factors that shape cutaneous pathological scarring, especially keloid formation and aggravation. They include circulating cytokines, chemokines, growth factors, particular cell types, sex hormones, the systemic renin‐angiotensin system, and vitamin D, all of which directly shape the angiogenesis, inflammation, fibrosis, and remodeling in pathological scars. There are also several environmental factors that more indirectly influence pathological scar formation or progression, namely diet, smoking, psychological stress, and exercise. Notably, much of the evidence on these systemic factors focus on their effects on one pathological scar characteristic, namely their fibrosis. However, systemic factors probably also shape other pathological scar characteristics. We describe two new avenues of keloid research that may greatly improve our understanding of pathological scarring and the systemic factors that affect it. One is the multiple similarities between keloids and tumors; the other is the different stem‐cell populations in keloids. We expect this research will greatly aid the development of diagnostic biomarkers for cutaneous pathological scars and drugs/techniques/regimens that prevent, improve, or cure these scars.

show abstract

Section: Vitamin Dmentioning

confidence: 99%

Systemic factors that shape cutaneous pathological scarring

Huang

Ogawa

2020

FASEB j.

View full text Add to dashboard Cite

show abstract

“…The major components of granulation tissue are macrophages, fibroblasts, proteoglycans, hyaluronic acid, collagen, and elastin. Platelet-derived growth factors (PDGF) and TGF-β released by macrophages activate fibroblasts and induce collagen III formation and the creation of an ECM (Gong et al 2017). With the upregulation of vascular endothelial growth factors (VEGF), angiogenesis is also initiated during this phase.…”

Section: Proliferationmentioning

confidence: 99%

Hypertrophic scars and keloids: a review and current treatment modalities

et al. 2020

View full text Add to dashboard Cite

Hypertrophic scars (HTS) are raised, red, rigid, inflexible cell-like, and cosmetic problems precipitated due to multiple underlying dermal injuries such as burn, surgery, and trauma during which aberrant wound healing with more pathological deposition of the extracellular matrix than degradation leads to their spawning. Till date, well established and specific treatments for HTS have not been reported; hence, the need of recent developments is thrusted with novel drug delivery vision. This review will try to encompass all the agogs to HTS, definition, pathophysiology, mechanism of hypertrophic scar formation, the role of growth factors in hypertrophic scarring, and their difference with keloids. Further, it will illuminate the available medicaments and recent advances in novel topical drug delivery systems such as ethosomes, transethosomes, liposomes, solid lipid nanoparticles, and microsponges for treatment of HTS.

show abstract

“…Individuals with KD are more likely to develop VD deficiency (VDD) (92), hypertension (3), and be dark-skinned (67). Both VDD and hypertension are also more prevalent in dark-skinned populations (67,92).…”

Section: Vitamin D Deficiency In Keloid Disordermentioning

confidence: 99%

“…The genes for plasminogen activator and VDR have been identified as susceptibility genes for KD (92).…”

Section: Vitamin D Deficiency In Keloid Disordermentioning

confidence: 99%

The Role of the Renin-Angiotensin System and Vitamin D in Keloid Disorder—A Review

et al. 2019

View full text Add to dashboard Cite

Keloid disorder (KD) is a fibroproliferative condition characterized by excessive dermal collagen deposition in response to wounding and/or inflammation of the skin. Despite intensive research, treatment for KD remains empirical and unsatisfactory. Activation of the renin-angiotensin system (RAS) leads to fibrosis in various organs through its direct effect and the resultant hypertension, and activation of the immune system. The observation of an increased incidence of KD in dark-skinned individuals who are predisposed to vitamin D deficiency (VDD) and hypertension, and the association of KD with hypertension and VDD, all of which are associated with an elevated activity of the RAS, provides clues to the pathogenesis of KD. There is increasing evidence implicating embryonic-like stem (ESC) cells that express ESC markers within keloid-associated lymphoid tissues (KALTs) in keloid lesions. These primitive cells express components of the RAS, cathepsins B, D, and G that constitute bypass loops of the RAS, and vitamin D receptor (VDR). This suggests that the RAS directly, and through signaling pathways that converge on the RAS, including VDR-mediated mechanisms and the immune system, may play a critical role in regulating the primitive population within the KALTs. This review discusses the role of the RAS, its relationship with hypertension, vitamin D, VDR, VDD, and the immune system that provide a microenvironmental niche in regulating the ESC-like cells within the KALTs. These ESC-like cells may be a novel therapeutic target for the treatment of this enigmatic and challenging condition, by modulating the RAS using inhibitors of the RAS and its bypass loops and convergent signaling pathways.

show abstract

Association of plasminogen activator inhibitor‐1 and vitamin D receptor expression with the risk of keloid disease in a Chinese population

Cited by 14 publications

References 29 publications

Systemic factors that shape cutaneous pathological scarring

Systemic factors that shape cutaneous pathological scarring

Hypertrophic scars and keloids: a review and current treatment modalities

The Role of the Renin-Angiotensin System and Vitamin D in Keloid Disorder—A Review

Contact Info

Product

Resources

About