About

Dr. Luis Andres Garza is a professor of dermatology at the Johns Hopkins University School of Medicine. His clinical expertise includes hidradenitis suppurativa, alopecia areata, and general dermatology. He received his undergraduate degree in neurobiology from Cornell University and earned both his M.D. and Ph.D. through the medical scientist training program at the University of Pennsylvania School of Medicine. Dr. Garza completed his dermatology residency at the University of Michigan and a fellowship at the University of Pennsylvania. He joined the Johns Hopkins faculty in 2009. In addition to his clinical practice, Dr. Garza runs a molecular biology laboratory focused on studying skin stem cells and wound healing. His research emphasizes identifying next-generation wound therapeutics and diagnostics, investigating how skin identity is maintained and manipulated, and understanding the processes involved in skin regeneration and healing. His work aims to provide insights that could improve patient care and advance the understanding of skin biology, regeneration, and stem cell biology.

Research topics

• Immunology
• Medicine
• Dermatology
• Cell biology
• Bioinformatics
• Biology
• Microbiology

Selected publications

• RNase L represses hair follicle regeneration through altered innate immune signaling

  Journal of Clinical Investigation · 2025-02-04 · 3 citations

  articleOpen accessSenior author

  Mammalian injury responses are predominantly characterized by fibrosis and scarring rather than functional regeneration. This limited regenerative capacity in mammals could reflect a loss of proregeneration programs or active suppression by genes functioning akin to tumor suppressors. To uncover programs governing regeneration in mammals, we screened transcripts in human participants following laser rejuvenation treatment and compared them with mice with enhanced wound-induced hair neogenesis (WIHN), a rare example of mammalian organogenesis. We found that Rnasel-/- mice exhibit an increased regenerative capacity, with elevated WIHN through enhanced IL-36α. Consistent with RNase L's known role to stimulate caspase-1, we found that pharmacologic inhibition of caspases promoted regeneration in an IL-36-dependent manner in multiple epithelial tissues. We identified a negative feedback loop, where RNase L-activated caspase-1 restrains the proregenerative dsRNA-TLR3 signaling cascade through the cleavage of toll-like adaptor protein TRIF. Through integrated single-cell RNA-seq and spatial transcriptomic profiling, we confirmed OAS & IL-36 genes to be highly expressed at the site of wounding and elevated in Rnasel-/- mouse wounds. This work suggests that RNase L functions as a regeneration repressor gene, in a functional trade off that tempers immune hyperactivation during viral infection at the cost of inhibiting regeneration.

  PublisherOA PDFDOI

• Plastic associated endocrine disruptors reduce Nicastrin protein and potentiate inflammation in hidradenitis suppurativa skin disease

  Nature Communications · 2025-11-28 · 1 citations

  articleOpen accessSenior authorCorresponding

  Hidradenitis Suppurativa (HS) is an inflammatory skin disorder with limited treatments and unclear etiology. While monogenic HS is linked to gamma secretase mutations, particularly in the NCSTN subunit, the pathogenesis of the more common sporadic form remains uncertain, though associated with risk factors such as diets high in ultra-processed foods. Consistent with the clinical overlap between sporadic and monogenic HS, we find loss of NCSTN protein in sporadic HS fibroblasts. We hypothesize the rising incidence of sporadic HS and its hormonal associations implicate endocrine-disrupting chemicals, especially plastic-associated EDCs (p-EDs) common in UPFs. We detect elevated p-ED adducts in HS skin, persisting in ex vivo cultured fibroblasts. At nanomolar concentrations, p-EDs inhibits NCSTN and primes fibroblasts for inflammation, mimicking NCSTN knockdown. These findings suggest p-ED exposure contributes to HS pathogenesis, highlighting the need to address environmental exposures in HS and other gamma secretase-related diseases.

  PublisherOA PDFDOI

• The mechanotransducer Piezo1 coordinates metabolism and inflammation to promote skin growth

  Nature Communications · 2025-07-25 · 14 citations

  articleOpen accessSenior author

  The skin has a remarkable ability to grow under constant stretch. Using a controlled tissue expansion system in mice, we identified an enhanced inflammatory-metabolic network in stretched skin via single-cell RNA sequencing, flow cytometry and spatial transcriptomics. Stretched epidermal cells exhibit heightened cellular crosstalk of CXCL, CCL, TNF, and TGF-β signaling. Additionally, skin expansion increases macrophage and monocyte infiltration in the skin while altering systemic immune cell profiles. Glycolysis-related genes, including Glut1 and Aldoa were significantly elevated. We hypothesize that Piezo1, a non-selective calcium-permeable cation channel, senses tension in stretched skin, driving these responses. The epidermal-Piezo1 loss-of-function animals show reduced skin growth, tissue weight, tissue thickness, macrophage infiltration, and glycolysis activity. Conversely, animals with a pharmacological Piezo1 gain of function exhibit an increase in these factors. Our findings highlight the coordinating role of Piezo1 for metabolic changes and immune cell infiltration in tension-induced skin growth. The skin has a remarkable ability to grow under stretch, though the underlying mechanisms remain unclear. Here, the authors show that the mechanosensor Piezo1 coordinates metabolic and immune responses to drive tension-induced skin growth.

  PublisherOA PDFDOI

• 0847 The addition of collagen scaffolds to human cell therapy to modify skin identity

  Journal of Investigative Dermatology · 2025-07-21

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Microbial homeostasis and dysbiosis in physiological and pathological skin

  Med · 2025-10-01 · 2 citations

  article
  PublisherDOI

• 0599 Plastic associated endocrine disruptors reduce nicastrin protein and potentiate inflammation in hidradenitis suppurativa

  Journal of Investigative Dermatology · 2025-07-21

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Use of an Intramolecular Quenched Fluorescence (IQF) Cleavage Assay for Assessing Enzyme Kinetics of Gamma-Secretase in Human Skin Fibroblasts and Keratinocytes

  Methods in molecular biology · 2025-01-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Pilot exploratory study to determine effect of fractionated CO2 laser to stimulate hair regrowth

  Journal of the American Academy of Dermatology · 2025-04-08

  articleOpen accessSenior author
  PublisherOA PDFDOI

• New Insights into the Neglected Disease Vulvar Lichen Sclerosus

  Journal of Investigative Dermatology · 2025-11-22

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Discovery of Orally Available Prodrugs of Itaconate and Derivatives

  Journal of Medicinal Chemistry · 2025-01-23 · 7 citations

  articleOpen access

  Itaconate, an endogenous immunomodulator from the tricarboxylic acid (TCA) cycle, shows therapeutic effects in various disease models, but is highly polar with poor cellular permeability. We previously reported a novel, topical itaconate derivative, SCD-153, for the treatment of alopecia areata. Here, we present the discovery of orally available itaconate derivatives for systemic and skin disorders. Four sets of prodrugs were synthesized using pivaloyloxymethyl (POM), isopropyloxycarbonyloxymethyl (POC), (5-methyl-2-oxo-1,3-dioxol-4-yl) methyl (ODOL), and 3-(hexadecyloxy)propyl (HDP) pro-moieties pairing with itaconic acid (IA), 1-methyl itaconate (1-MI), and 4-methyl itaconate (4-MI). Among these, POC-based prodrugs (P2, P9, P13) showed favorable stability, permeability, and pharmacokinetics. Notably, P2 and P13 significantly inhibited Poly(I:C)/IFNγ-induced inflammatory cytokines in human epidermal keratinocytes. Oral studies demonstrated favorable pharmacokinetics releasing micromolar concentrations of IA or 4-MI from P2 and P13, respectively. These findings highlight the potential of prodrug strategies to enhance itaconate’s cellular permeability and oral bioavailability, paving the way for clinical translation.

  PublisherOA PDFDOI

Recent grants

• Injection of autologous volar fibroblasts to the stump site to allow pressure adaptation and enhanced prosthetic use in amputees

  NIH · $532k · 2021–2023

• Mechanism and clinical pilot tst of volar fibroblast to create ectopic volar skin

  NIH · $1.8M · 2013–2019

• NIH Grant K08AR055666

  NIH · $633k · 2013

• Retinoic acid synthesis induced by noncoding dsRNA controls Regeneration

  NIH · $1.8M · 2019–2024

• Retinoic acid synthesis induced by noncoding dsRNA controls Regeneration

  NIH · $481k · 2019–2024

Frequent coauthors

• Lloyd Miller

  Johns Hopkins University

  174 shared

• Gaofeng Wang

  Nanfang Hospital

  93 shared

• David A. Rubenstein

  81 shared

• Nicholas A. Soter

  New York University

  81 shared

• Richard L. Gallo

  University of California, San Diego

  81 shared

• Mary‐Margaret Chren

  Vanderbilt University Medical Center

  81 shared

• Janssen Immunology

  Pfizer (United Kingdom)

  81 shared

• Tomoko Maeda‐Chubachi

  81 shared

Education

• B.S., Neurobiology

  Cornell University

• M.D.

  University of Pennsylvania School of Medicine

• Ph.D.

  University of Pennsylvania School of Medicine

Awards & honors

• Elected to American Society for Clinical Investigation (ASCI…
• Daniel Nathans Scholar at Johns Hopkins University School of…
• American Skin Association Research Achievement Award in Tran…