0B68 Iozzo, Renato V. - Thomas Jefferson University - Thomas Jefferson University
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Renato V. Iozzo, MD

Contact Dr. Iozzo

1020 Locust Street
Jefferson Alumni Hall, Suite 336A
Philadelphia, PA 19107

(215) 503-2208
(215) 923-7969 fax

Most Recent Peer-reviewed Publications

  1. Endorepellin evokes autophagy in endothelial cells
  2. Decorin induces mitophagy in breast carcinoma cells via peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and mitostatin
  3. Decorin activates AMPK, an energy sensor kinase, to induce autophagy in endothelial cells
  4. The injury response of aged tendons in the absence of biglycan and decorin
  5. FOXD1 promotes nephron progenitor differentiation by repressing decorin in the embryonic kidney
  6. Reprint of: Decorin activates AMPK, an energy sensor kinase, to induce autophagy in endothelial cells
  7. The tendon injury response is influenced by decorin and biglycan
  8. Decorin deficiency promotes hepatic carcinogenesis
  9. Instructive roles of extracellular matrix on autophagy
  10. Biglycan and decorin differentially regulate signaling in the fetal membranes
  11. The role of vascular-derived perlecan in modulating cell adhesion, proliferation and growth factor signaling
  12. Osteoblastic cell secretome: A novel role for progranulin during risedronate treatment
  13. A decorin-deficient matrix affects skin chondroitin/dermatan sulfate levels and keratinocyte function
  14. Key roles for the small leucine-rich proteoglycans in renal and pulmonary pathophysiology
  15. De novo expression of circulating biglycan evokes an innate inflammatory tissue response via MyD88/TRIF pathways
  16. Decorin differentially modulates the activity of insulin receptor isoform A ligands
  17. Biglycan-triggered TLR-2- and TLR-4-signaling exacerbates the pathophysiology of ischemic acute kidney injury
  18. The location-specific role of proteoglycans in the flexor carpi ulnaris tendon
  19. Decorin has an appetite for endothelial cell autophagy
  20. Decorin causes autophagy in endothelial cells via Peg3
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