About

Ryan C. Branski, PhD, is a professor in the Department of Otolaryngology-Head and Neck Surgery and the Department of Rehabilitation Medicine at NYU Grossman School of Medicine. His research focuses on developing and optimizing therapeutic approaches for diseases of the upper aerodigestive tract that manifest as speech, voice, and swallowing disorders, which result in disability and diminished quality of life. Dr. Branski's laboratory employs regenerative medicine and tissue engineering approaches, including gene therapy delivery to the vocal folds and tissue engineering constructs, to address functional deficits affecting communication and deglutition. He has pioneered these techniques and his work is funded by the National Institutes of Health. Dr. Branski has published over 130 peer-reviewed manuscripts and edited four books. He is recognized as a fellow of the American Speech Language Hearing Association, the American Laryngological Association, and the Academy of Otolaryngology-Head and Neck Surgery. His contributions significantly advance the understanding and treatment of voice and swallowing disorders.

Research topics

• Medicine
• Internal medicine
• Biology
• Surgery
• Pathology

Selected publications

• <scp>TGFβ</scp> /Smad2/3‐Mediated Crosstalk Between Vocal Fold Fibroblasts and Myoblasts In Vitro

  The Laryngoscope · 2026-01-14

  articleSenior author

  OBJECTIVES: Traditionally, disorders of the vocal fold (VF) mucosa and underlying musculature have been regarded as mutually exclusive entities. However, emerging evidence from other organ systems suggests mucosal and muscle compartments engage in reciprocal interactions with functional consequences. We hypothesized that similar crosstalk exists in the VF, whereby fibrotic mucosa influences adjacent muscle. To model this process, we stimulated human VF fibroblasts (HVOX) with TGF-β1, a central mediator of fibrosis, and examined the effects on rat VF myoblasts (rVF-Mbs), as well as reciprocal influences of rVF-Mbs on fibroblasts. METHODS: HVOX fibroblasts were stimulated with 10 ng/mL TGF-β1, and the effects on rVF-Mbs were assessed using conditioned media and co-culture. Myotube formation was evaluated by immunofluorescence, and nuclear localization of Smad2/3 was examined in conditioned media experiments. qRT-PCR quantified transcripts related to myogenic differentiation and Smad2/3 signaling. ALK4/5 inhibition was performed in co-culture to test TGF-β/Smad2/3-signaling pathway involvement. Reciprocal effects were examined by changes in fibrogenic gene expression in HVOX fibroblasts. RESULTS: Both conditioned media and co-culture suppressed myogenic differentiation in rVF-Mbs; increased inhibition was observed in co-culture, as indicated by reduced myotube formation, decreased Myh2 expression, and activation of Smad2/3 signaling. ALK4/5 inhibition abrogated these effects. Differentiating rVF-Mbs attenuated the fibrogenic phenotype of HVOX fibroblasts. CONCLUSIONS: Fibrotic VF mucosal cells can impair myogenic differentiation through TGF-β/Smad2/3-mediated fibroblast-myoblast crosstalk, and myogenic cells may exert reciprocal anti-fibrotic effects. These findings suggest mucosa-muscle interactions may contribute to VF pathology and highlight Smad2/3 as a potential therapeutic target. LEVEL OF EVIDENCE: NA STUDY DESIGN: In vitro.

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• Perceptions of the Effect of Habits on Vocal Health: Comparing Healthcare Providers to Vocalists

  Journal of Voice · 2026-01-01

  article
  PublisherDOI

• YAP/TAZ inhibition refines TGF-β signaling to prevent laryngeal fibrosis

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-21

  articleOpen accessSenior author

  Voice disorders affect nearly 20 million Americans and cost more than $13 billion annually. Vocal fold (VF) fibrosis, a major cause of chronic dysphonia, disrupts normal vocal fold vibration by replacing the flexible extracellular matrix with stiff fibrotic tissue. Although TGF-β drives fibrosis, it also activates intrinsic negative feedback mechanisms, including SMAD7 induction and SMAD3 downregulation, to restrain excessive signaling. Broad inhibition of TGF-β or canonical SMAD signaling may disrupt these protective feedback loops and impair normal tissue homeostasis. An ideal anti-fibrotic strategy should differentially target the pro-fibrotic output of TGF-β. Here, we show YAP/TAZ inhibition selectively suppresses pro-fibrotic TGF-β signaling in VF fibroblasts. Pharmacologic inhibition of YAP/TAZ blocked TGF-β-induced fibroblast activation and fibrotic gene expression, while only modestly affecting canonical SMAD feedback responses. Integrated RNA-seq and ChIP-seq analyses demonstrated YAP/TAZ primarily regulate non-canonical TGF-β signaling and pro-fibrotic transcriptional programs. In a rat model of VF fibrosis, YAP/TAZ inhibition reduced nuclear YAP/TAZ localization and attenuated scar formation. Together, these findings identify YAP/TAZ inhibition as a promising therapeutic strategy for VF fibrosis and other fibrotic diseases.

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• Transmuscular vocal fold injury reduces frequency complexity of rat ultrasonic vocalizations

  Behavioural Brain Research · 2025-12-08

  articleOpen access
  PublisherOA PDFDOI

• An Observational Study of the Prevalence of Oral Human Papilloma Virus Infection in Laryngologists

  The Laryngoscope · 2025-07-30

  article

  ABSTRACT Objective Surgical treatment of recurrent respiratory papillomatosis (RRP) has been shown to aerosolize human papillomavirus (HPV), putting healthcare workers at risk for exposure, infection, and disease. Knowledge of HPV infection risk among otolaryngologists who treat HPV‐related diseases is limited. We sought to characterize the prevalence of oral HPV infection in otolaryngologists treating RRP. Methods This observational cohort study enrolled otolaryngologists at a national meeting. Participants completed a survey concerning HPV vaccination, disease history, and practice techniques for patients with RRP. An oral rinse was collected from participants; DNA was extracted and analyzed using commercially available kits. Results A total of 137 participants were included with an average age of 42 years (SD 11); 86 participants (63%) were female. A history of HPV‐related infections, such as cutaneous warts, was reported by 38 participants (28%). About half of the participants ( N = 77, 56%) were vaccinated against HPV. Multiple techniques for managing RRP were reported, including KTP laser ( N = 107), CO 2 laser ( N = 78), microdebrider ( N = 80), and cold steel ( N = 21). Oral rinses from three participants (2.2%) tested positive for HPV, including Subtypes 6 ( N = 2) and 16 ( N = 1). All three were male with no history of HPV vaccination. Conclusion Otolaryngologists treating HPV‐related diseases do not seem to be at a higher risk of HPV infection compared to the general adult population. Vaccination, the use of N95 masks, and minimizing aerosol‐generating techniques are likely protective for healthcare workers dealing with HPV‐related conditions. Level of Evidence 3.

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• Porcine Vocal Fold Lamina Propria-Derived Biomaterials Modulate TGF-β1-Mediated Fibroblast Activation in Vitro

  UNC Libraries · 2025-07-24

  articleOpen access

  The vocal fold lamina propria (VFLP), one of the outermost layers of the vocal fold (VF), is composed of tissue-specific extracellular matrix (ECM) proteins and is highly susceptible to injury. Various biomaterials have been clinically tested to treat voice disorders (e.g., hydrogels, fat, and hyaluronic acid), but satisfactory recovery of the VF functionality remains elusive. Fibrosis or scar formation in the VF is a major challenge, and the development and refinement of novel therapeutics that promote the healing and normal function of the VF are needed. Injectable hydrogels derived from native tissues have been previously reported with major advantages over synthetic hydrogels, including constructive tissue remodeling and reduced scar tissue formation. This study aims to characterize the composition of a decellularized porcine VFLP-ECM scaffold and the cytocompatibility and potential antifibrotic properties of a hydrogel derived from VFLP-ECM. In addition, we isolated potential matrix-bound vesicles (MBVs) and macromolecules from the VFLP-ECM that also downregulated smooth muscle actin <em>ACTA2</em> under transforming growth factor-beta 1 (TGF-&beta;1) stimulation. The results provide evidence of the unique protein composition of the VFLP-ECM and the potential link between the components of the VFLP-ECM and the inhibition of TGF-&beta;1 signaling observed in vitro when transformed into injectable forms.

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• Smad2/3 Signaling Mediates the Atrophic Response in Vocal Fold Myoblasts In Vitro

  The Laryngoscope · 2025-07-30 · 1 citations

  articleOpen accessSenior author

  BACKGROUND/OBJECTIVES: Vocal fold (VF) muscle atrophy, often associated with neuromuscular disorders and aging, can lead to voice-related disability. Myostatin is well-known to mediate skeletal muscle atrophy via Smad2/3 signaling, whereas TGF-β1, a potent inducer of Smad2/3 signaling, is upregulated following VF injury. However, the impact of Smad2/3 signaling on laryngeal muscles remains unclear. This study provides foundational insight regarding Smad2/3-dependent atrophic responses of VF skeletal muscle cells, to ultimately develop novel therapeutic strategies for VF muscle atrophy. STUDY DESIGN: In vitro. METHODS: Myoblasts isolated from the rat thyroarytenoid muscle were differentiated into myotubes in myogenic differentiation medium ±500 ng/mL myostatin or 10 ng/mL TGF-β1, in the presence or absence of an ALK4/5 inhibitor or siRNA targeting Smad2 and Smad3. Myotube formation and activation of Smad2/3 (nuclear localization of Smad2/3) were assessed via immunofluorescence. Transcription related to myotube differentiation and Smad2/3 signaling was quantified by qRT-PCR. RESULTS: Both myostatin and TGF-β1 suppressed myogenic differentiation, increased Smad2/3 nuclear intensity, downregulated Myh2, and upregulated downstream targets of Smad2/3 (Ccn2 and Serpine1) and Fbox32, an atrophy-related gene. These effects were more pronounced with TGF-β1 than with myostatin and were reversed by inhibition of ALK4/5. Furthermore, Smad2/3 knockdown via siRNA promoted myogenic differentiation, further supporting the role of Smad2/3 signaling in the atrophic response in VF myoblasts. CONCLUSIONS: Smad2/3 signaling mediates differentiation of VF myoblasts and TGF-β1, a potent mediator of fibrosis, elicited a more pronounced atrophic response than myostatin. Smad2/3 may be an attractive therapeutic target for VF muscle atrophy. LEVEL OF EVIDENCE: NA.

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• Patient Perception of Vocal Tremor Severity and its Relationship to Acoustic Voice Outcomes: An Exploratory Study

  Tremor and Other Hyperkinetic Movements · 2025-01-01

  articleOpen accessSenior author

  Background: Vocal tremor profoundly impacts communication, social participation, and quality of life. Although expert auditory-perceptual ratings of vocal tremor severity align with acoustic voice outcomes (e.g., extent of frequency (fo) and intensity modulation), patient perception of their voice remains unexamined despite its clinical importance. This study aimed to characterize the relationship between patient-reported vocal tremor severity and acoustic voice outcomes at baseline and after botulinum toxin injections. Method: Patients diagnosed with vocal tremor affecting multiple structures (ETvt) or tremor only observed in the larynx (LDvt) were recruited. Participants completed the voice section of the Quality of Life in Essential Tremor questionnaire to assess patient perception and performed sustained /ɑ/ at a comfortable pitch and volume, from which acoustic voice outcomes (rate and extent of fundamental frequency [fo] and amplitude [dB] modulation) were derived. A subset of participants received botulinum toxin injections and were reassessed within the therapeutic window (within 12 weeks). Results: Thirty participants (29 females; mean age = 72 years, SD = 11.40) were analyzed. Participants who rated their vocal tremor as “severe” demonstrated higher rate fo (β = 1.20, 95% CI: –0.10, 2.60 Hz) and rate dB (β = 2.30, 95% CI: 0.50, 4.10 Hz) compared to participants who rated their tremor as “moderate”. Participants who rated their tremor as “marked” demonstrated higher rate fo (β = 1.50, 95% CI: 0.30, 2.60 Hz) compared to “moderate” ratings. Improvements in patient perception of vocal tremor and acoustic outcomes were highly heterogenous among seven participants who received botulinum toxin. Discussion: Participants reporting more severe vocal tremor demonstrated more aberrant acoustic voice outcomes. After botulinum toxin injection, substantial heterogeneity was observed in acoustic voice measures which varied based on patient perception of change. These preliminary, exploratory findings provide a foundation for future investigations to define meaningful change in this population.

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• Injection of vocal fold lamina propria-derived hydrogels modulates fibrosis in injured vocal folds

  Biomaterials Advances · 2025-07-24 · 6 citations

  articleOpen access

  Vocal fold (VF) fibrosis, often resulting from phonosurgery, radiation, or trauma, causes irreversible voice dysfunction due to excessive ECM deposition and increased tissue stiffness. No FDA-approved treatments for VF fibrosis exist, highlighting the need for novel antifibrotic therapies. TGF-β1 contributes to fibroblast-to-myofibroblast activation, leading to increased ACTA2 expression and collagen production via SMAD3, YAP1, and integrin signaling pathways. Leveraging the principle that local cells respond to tissue-specific signals, our ECM hydrogel, derived from decellularized vocal fold lamina propria (VFLP-ECM), reduced ACTA2 expression in TGF-β1-stimulated VF fibroblasts, showcasing antifibrotic potential. This study evaluates the therapeutic potential of VFLP-ECM hydrogel in a rabbit VF injury model. VFLP-ECM hydrogel or bovine type I collagen injections were administered 7 days post-injury and evaluated on day 28. We compared two VFLP-ECM formulations: a manual process (VFLP (man)) and an accelerated automated method (VFLP (au)). VFLP (man) modulated fibrosis-associated gene expressions more effectively than controls. Proteomics identified 229 proteins uniquely preserved in VFLP (man), including vitronectin, crucial in TGF-β1 signaling and ECM remodeling. Transcriptomic analysis suggests downregulation of fibrotic markers and inhibition of SMAD3, YAP1, and MRTFA, alongside upregulation of SMAD7, an inhibitor of TGF-β signaling. Notably, VFLP (man) treatment recovered stiffness comparable to uninjured controls (1.84 vs. 1.94 mN), whereas collagen-treated tissues remained stiff (2.7 mN), similar to the injury group (2.6 mN), indicating incomplete mechanical recovery. These in vivo data show that manually decellularized VFLP-ECM hydrogel attenuates fibrosis by disrupting key biochemical and mechanical cues driving myofibroblast activation. • Tissue-specific VFLP-ECM hydrogel restores vocal fold mechanics in vivo 28 days after injury. • VFLP-ECM hydrogel shows improved vocal fold repair compared to type I collagen. • Proteomic analysis indicates that matrisome proteins like vitronectin may drive the in vivo response. • Transcriptomic data reveal that ECM hydrogel inhibits fibrosis through non-canonical mechanisms.

  PublisherDOI

• Fast Automated Approach for the Derivation of Acellular Extracellular Matrix Scaffolds from Porcine Soft Tissues

  UNC Libraries · 2025-07-24

  articleOpen access

  Decellularized extracellular matrix (ECM) scaffolds derived from tissues and organs are complex biomaterials used in clinical and research applications. A number of decellularization protocols have been described for ECM biomaterials derivation, each adapted to a particular tissue and use, restricting comparisons among materials. One of the major sources of variability in ECM products comes from the tissue source and animal age. Although this variability could be minimized using established tissue sources, other sources arise from the decellularization process itself. Overall, current protocols require manual work and are poorly standardized with regard to the choice of reagents, the order by which they are added, and exposure times. The combination of these factors adds variability affecting the uniformity of the final product between batches. Furthermore, each protocol needs to be optimized for each tissue and tissue source making tissue-to-tissue comparisons difficult. Automation and standardization of ECM scaffold development constitute a significant improvement to current biomanufacturing techniques but remains poorly explored. This study aimed to develop a biofabrication method for fast and automated derivation of raw material for ECM hydrogel production while preserving ECM composition and controlling lot-to-lot variability. The main result was a closed semibatch bioreactor system with automated dosing of decellularization reagents capable of deriving ECM material from pretreated soft tissues. The ECM was further processed into hydrogels to demonstrate gelation and cytocompatibility. This work presents a versatile, scalable, and automated platform for the rapid production of ECM scaffolds.

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Recent grants

• NIH Grant R03DC010267

  NIH · $520k · 2012

• NIH Grant F31DC006764

  NIH · $26k · 2005

• Optimal RNA-based therapeutics for vocal fold injury and fibrosis

  NIH · $2.3M · 2014–2020

• Multiple mechanisms underlying GR-mediated therapies for fibroplasia of the vocal folds

  NIH · $2.6M · 2018–2024

Frequent coauthors

• Milan R. Amin

  New York University

  76 shared

• Renjie Bing

  New York University

  30 shared

• Gregory R. Dion

  University of Cincinnati

  26 shared

• Dennis H. Kraus

  24 shared

• Patricia A. Hebda

  University of Pittsburgh

  22 shared

• Stuart D. Katz

  New York University

  21 shared

• Grace A. McComsey

  Case Western Reserve University

  20 shared

• Andrea S. Foulkes

  18 shared

Labs

• Branski LaboratoryPI

Awards & honors

• Fellow of the American Speech Language Hearing Association
• Fellow of the American Laryngological Association
• Fellow of the Academy of Otolaryngology-Head and Neck Surger…