Contact

  • Academic
    sdavala@stanford.edu
    University - Scholar Department: Pediatrics Position: Medical Fellow

All Publications

  • Current opinion in pediatrics: pediatric lung transplantation in the 21st century. Current opinion in pediatrics Davala, S., Si, X. 2026

    Abstract

    This review provides a summary of the evolving landscape of pediatric lung transplantation highlighting current trends, short and long-term outcomes, ongoing challenges in posttransplant survival, and unique considerations in pediatric populations.The annual volume of pediatric lung transplantation has declined over the past decade due to a decreased need among children with cystic fibrosis. Improvement in survival has paralleled advancements in bridge to transplant strategies, expanding what were once considered contraindications. Despite the ongoing shortage of donor organs, innovations in policy changes, surgical and immunologic strategies, and organ preservation technologies have expanded the donor lung pool. Chronic lung allograft dysfunction (CLAD) remains the primary limitation to long-term survival, with limited management strategies and emerging immunomodulatory therapies offering promise.As survival in pediatric lung transplantation improves, emphasis should shift to long-term outcomes including quality of life and equitable care, development of effective CLAD prevention strategies and pediatric-specific guidelines to optimize long-term survival.

    View details for DOI 10.1097/MOP.0000000000001572

    View details for PubMedID 41983738

  • Inhibition of TET1 prevents the development of osteoarthritis and reveals the 5hmC landscape that orchestrates pathogenesis. Science translational medicine Smeriglio, P. n., Grandi, F. C., Davala, S. n., Masarapu, V. n., Indelli, P. F., Goodman, S. B., Bhutani, N. n. 2020; 12 (539)

    Abstract

    Osteoarthritis (OA) is a degenerative disease of the joint, which results in pain, loss of mobility, and, eventually, joint replacement. Currently, no disease-modifying drugs exist, partly because of the multiple levels at which cartilage homeostasis is disrupted. Recent studies have highlighted the importance of epigenetic dysregulation in OA, sparking interest in the epigenetic modulation for this disease. In our previous work, we characterized a fivefold increase in cytosine hydroxymethylation (5hmC), an oxidized derivative of cytosine methylation (5mC) associated with gene activation, accumulating at OA-associated genes. To test the role of 5hmC in OA, here, we used a mouse model of surgically induced OA and found that OA onset was accompanied by a gain of ~40,000 differentially hydroxymethylated sites before the notable histological appearance of disease. We demonstrated that ten-eleven-translocation enzyme 1 (TET1) mediates the 5hmC deposition because 98% of sites enriched for 5hmC in OA were lost in Tet1-/- mice. Loss of TET1-mediated 5hmC protected the Tet1-/- mice from OA development, including degeneration of the cartilage surface and osteophyte formation, by directly preventing the activation of multiple OA pathways. Loss of TET1 in human OA chondrocytes reduced the expression of the matrix metalloproteinases MMP3 and MMP13 and multiple inflammatory cytokines. Intra-articular injections of a dioxygenases inhibitor, 2-hydroxyglutarate, on mice after surgical induction of OA stalled disease progression. Treatment of human OA chondrocytes with the same inhibitor also phenocopied TET1 loss. Collectively, these data demonstrate that TET1-mediated 5hmC deposition regulates multiple OA pathways and can be modulated for therapeutic intervention.

    View details for DOI 10.1126/scitranslmed.aax2332

    View details for PubMedID 32295898