Kelly X Huang

All Publications

• Clinical Features and Mechanisms of Differential Wound Healing and Scarring Across Anatomical Sites Advances in Wound Care Yao, H., Jing, S., Huang, K., Griffin, M., Longaker, M., Wan, D., Li, D. 2025

  Abstract

  Significance: Fibrosis is associated with high rates of morbidity and mortality and poses a heavy burden on the health care system. Different regions of the body heal at different rates with varying degrees of fibrosis, with regions such as the extremities and trunk being more prone to scarring than the face and mucosa. Therapies that leverage the unique mechanisms underlying these anatomical differences in wound healing may be effective in mitigating fibrosis and scarring. Recent Advances: Recent studies in mice have revealed fibroblast-intrinsic signaling pathways that contribute to scar formation in different areas of the body, such as engrailed-1-positive fibroblasts and paired-related homeobox-1-positive fibroblasts in dorsal, ventral, and dermal scars, respectively. Novel approaches that target specific molecular pathways within fibroblasts may pave the way for effective therapies in replicating features of scar-resistant skin and facilitating wound healing. Critical Issues: Clinical practice and animal studies have shown some body regions to be more susceptible to fibrosis than others. However, our understanding on cellular and molecular mechanisms that contribute to this phenomenon remains limited. Future Directions: Advances in antiscarring therapy will benefit from harnessing several aspects of wound healing in regions less prone to fibrosis, including reducing mechanical tension, controlling angiogenic response, and modulating fibroblast subtypes. [Figure: see text] [Figure: see text].

  View details for DOI 10.1177/21621918251387627

• Biomaterial Cues for Regulation of Osteoclast Differentiation and Function in Bone Regeneration ADVANCED THERAPEUTICS Shariati, K., Bedar, M., Huang, K. X., Moghadam, S., Mirzaie, S., LaGuardia, J. S., Chen, W., Kang, Y., Ren, X., Lee, J. C. 2024

  View details for DOI 10.1002/adtp.202400296

  View details for Web of Science ID 001357286300001

• Correlating Material Properties to Osteoprotegerin Expression on Nanoparticulate Mineralized Collagen Glycosaminoglycan Scaffolds ADVANCED HEALTHCARE MATERIALS Chen, W., Bedar, M., Zhou, Q., Ren, X., Kang, Y., Huang, K. X., Rubino, G., Kolliopoulos, V., Moghadam, S., Cascavita, C. T., Taylor, J. M., Chevalier, J. M., Harley, B. A. C., Lee, J. C. 2024; 13 (26): e2401037

  Abstract

  Precision material design directed by cell biological processes represents a frontier in developing clinically translatable regenerative technologies. While understanding cell-material interactions on multipotent progenitor cells yields insights on target tissue differentiation, equally if not more important is the quantification of indirect multicellular interactions. In this work, the relationship of two material properties, phosphate content and stiffness, of a nanoparticulate mineralized collagen glycosaminoglycan scaffold (MC-GAG) in the expression of an endogenous anti-osteoclastogenic secreted protein, osteoprotegerin (OPG) by primary human mesenchymal stem cells (hMSCs) is evaluated. The phosphate content of MC-GAG requires the type III sodium phosphate symporter PiT-1/SLC20A1 for OPG expression, correlating with β-catenin downregulation, but is independent of the effects of phosphate ion on osteogenic differentiation. Using three stiffness MC-GAG variants that do not differ significantly by osteogenic differentiation, it is observed that the softest material elicited ≈1.6-2 times higher OPG expression than the stiffer materials. Knockdown of the mechanosensitive signaling axis of YAP, TAZ, β-catenin and combinations thereof in hMSCs on MC-GAG demonstrates that β-catenin downregulation increases OPG expression by 1.5-fold. Taken together, these data constitute a roadmap for material properties that can used to suppress osteoclast activation via osteoprotegerin expression separately from the anabolic processes of osteogenesis.

  View details for DOI 10.1002/adhm.202401037

  View details for Web of Science ID 001253840000001

  View details for PubMedID 38885525

  View details for PubMedCentralID PMC11489015

• Bone-Anchored Maxillary Protraction for Adolescents with Cleft Palate and Class III Malocclusion: A Case Series CLEFT PALATE CRANIOFACIAL JOURNAL Chin, M. G., Gishen, K. E., Bedar, M., Huang, K. X., Laguardia, J. S., Moghadam, S., Lee, J. C., Panchura, J., Wilson, L. F. 2025; 62 (1): 13-20

  Abstract

  To describe the long-term treatment course of bone-anchored maxillary protraction (BAMP) and evaluate orthognathic surgical indications after BAMP. Retrospective case series. Craniofacial/Cleft Palate Program at the Orthopaedic Institute for Children in Los Angeles, CA. Twelve male patients with cleft palate (CP), unilateral cleft lip and palate (UCLP), or bilateral cleft lip and palate (BCLP) and Class III malocclusion treated with BAMP (mean age: 11.4 ± 2.6 years) were included. BAMP treatment was performed by placement of bone-anchored maxillary and mandibular plates connected with intraoral Class III dental elastics or maxillary plates connected to a facemask. We retrospectively assessed BAMP treatment variables, including age at surgery, revision surgeries, and treatment duration. The primary goal was correction to class I occlusion. Twelve patients underwent BAMP treatment for an average of 4.4 ± 2.4 years. Two patients were corrected to class I occlusion at the time of this report. Le Fort I advancement was no longer required in two patients (16.7%), it was required for nine patients (75.0%) and was completed for one patient following BAMP treatment (8.3%). This preliminary report demonstrated that BAMP treatment may be associated with a minimal reduction in the requirement for Le Fort I advancement at skeletal maturity. Future studies with larger sample sizes are necessary to confirm this association.

  View details for DOI 10.1177/10556656231219439

  View details for Web of Science ID 001125845400001

  View details for PubMedID 38086751