John Evankovich III, MD

  • Associate Professor of Medicine
  • Associate Professor in Environmental and Occupational Health
  • Medical Director, UPMC Jameson ICU
Academic Interests

Dr. Evankovich studies the molecular biology of lung injury. His laboratory is interested in the intersection of three molecular systems in the innate immune system, and how they influence inflammation and cell death pathways in the lung. The molecular systems are Damage Associated Molecular Patterns (DAMPs), DAMP Receptors, and the Ubiquitin/Proteasome System (UPS).

Dr. Evankovich's prior work has identified how several novel DAMP/DAMP receptor pairs are processed for disposal in the UPS, and how this process can be manipulated to change subsequent cellular responses. For damaging responses, increasing targeted DAMP receptor disposal through the UPS could lessen organ damage; likewise, for protective DAMP/DAMP receptor pairs, reducing disposal in the UPS could be therapeutic to reduce injury. Teaming with the Small Molecule Therapeutics Center, Dr. Evankovich's future work aims to discover novel small molecules to disrupt these pathways and test in preclinical models of lung injury. He is also an Associate Member of the Aging Institute, where he focuses on the contribution of aging to innate immune responses in the lung.

Dr. Evankovich attends in the Medical Intensive Care Units at UPMC East and UPMC Presbyterian, where he cares for critically-ill patients with respiratory failure, sepsis, among others. He is particularly interested in the care of patients with Acute Respiratory Distress Syndrome - a form of respiratory failure with features of severe inflammation.

Dr. Evankovich is active in bedside critical care and procedural educational activities for housestaff in the UPMC Presbyterian and McKeesport Internal Medicine Residency Programs.

    Education & Training

  • BS, Biotechnology and Biology, Gannon University, 2007
  • MD, University of Pittsburgh School of Medicine, 2012
  • Residency, Internal Medicine, University of Pittsburgh School of Medicine, 2014
  • Fellowship, Pulmonary, Allergy & Critical Care Medicine, University of Pittsburgh School of Medicine, 2018
Recent Publications

Evankovich J, Lear T, Baldwin C, Chen Y, White V, Villandre J, ...& Mallampalli RK. Toll-like receptor 8 stability is regulated by ring finger 216 in response to circulating microRNAs. American Journal of Respiratory Cell and Molecular Biology. 2020; 62(2): 157-167.

Tong Y*, Lear TB*, Evankovich J*, Chen Y, Londino JD, Myerburg MM, ...& Lockwood KC. The RNFT2/IL-3RĂ¡ axis regulates IL-3 signaling and innate immunity. JCI Insight. 2020; 5(3)

Chen Y, Evankovich JW, Lear TB, Tuncer F, Kennerdell JR, Camarco DP, ...Chen BB. A small molecule NRF2 activator BC-1901S ameliorates inflammation through DCAF1/NRF2 axis. Redox Biology. 2020; 101485

Evankovich J, Lear T, McKelvey A, Dunn S, Londino J, Liu Y, ...& Mallampalli RK. Receptor for advanced glycation end products is targeted by FBXO10 for ubiquitination and degradation. The FASEB Journal. 2017; 31(9): 3894-3903.

McKelvey AC, Lear TB, Dunn SR, Evankovich J, Londino JD, Bednash JS, ...& Chen BB. RING finger E3 ligase PPP1R11 regulates TLR2 signaling and innate immunity. Elive. 2016; 5: e18496.

Huang H, Chen HW, Evankovich J, Yan W, Rosborough BR, Nace GW, ...& Esmon CT. Histones activate the NLRP3 inflammasome in Kupffer cells during sterile inflammatory liver injury. The Journal of Immunology. 2013; 191(5): 2665-2679.

Evankovich J, Zhang R, Cardinal JS, Zhang L, Chen J, Huang H, ...& Tsung A. Calcium/calmodulin-dependent protein kinase IV limits organ damage in hepatic ischemia-reperfusion injury through induction of autophagy. American Journal of Physiology-Gastrointestinal and Liver Physiology. 2012; 303(2): G189-G198.

Huang H, Evankovich J, Yan W, Nace G, Zhang L, Ross M, ...& Tsung A. Endogenous histones function as alarmins in sterile inflammatory liver injury through Toll like receptor 9 in mice. Hepatology. 2011; 54(3): 999-1008.

Evankovich J, Cho SW, Zhang R, Cardinal J, Dhupar R, Zhang L, ...& Tsung A. High mobility group box 1 release from hepatocytes during ischemia and reperfusion injury is mediated by decreased histone deacetylase activity. Journal of Biological Chemistry. 2010; 285(51): 39888-39897.

Evankovich J, Billiar T, Tsung A. Toll-like receptors in hepatic ischemia/reperfusion and transplantation. Gastroenterology Research and Practice. 2010

    Honors and Awards
  • Robert M. Rogers Award for Outstanding Scholars Achievement, 2018