A photo of Steve Standage.

Attending Physician, Pediatric Intensive Care Unit (PICU)

Assistant Professor, UC Department of Pediatrics

513-803-7685

Board Certified

My Biography & Research

Biography

I am a child at heart. I love kids, and most of my jobs growing up dealt with kids. But I love science, too, and I wanted to pursue laboratory-based research.

As I advanced in my studies and spent increasing amounts of time in the lab, I missed human interaction. I decided then that being a pediatrician would allow me to pursue my scientific interests while also applying them in a meaningful way as I cared for sick children and their families.

I chose pediatric critical care because I'm a tinkerer. I love to know how things work, and I love fixing them when they don't. Human physiology is intricate and amazing, but when it goes wrong, kids can get very sick. I love having the knowledge and tools to understand and fix that physiology in real-time in the intensive care unit (ICU) to help kids get better from life-threatening diseases.

Currently, I study sepsis and sepsis-induced organ failure, specifically how cellular metabolism changes in sepsis-associated heart and kidney failure. My research interests stem from a medical school rotation in the pediatric ICU. There, I helped care for two unrelated boys admitted to the hospital within 24 hours of each other, each with severe septic shock. Though their clinical presentations were very similar, one unfortunately succumbed to sepsis while the other recovered. I was intrigued, and I wanted to know why.

Since then, I have studied the fundamental mechanisms of sepsis to better understand how it works and what we, as doctors, can do to fix it. I want to do everything possible to prevent negative outcomes for children when they get sick.

My research focuses on the downstream effects of the inflammatory signals released by the immune system in response to significant infection. Sepsis causes the release of high levels of these inflammatory signals, which then influence cells to change how they function. In response, cells adapt their metabolism and alter what they do. Sepsis-associated organ failure is caused by cells that stop performing their normal functions.

My expectation is that, when we understand how inflammation changes cellular metabolism and function, we can design more targeted, effective treatments to reverse the pathological cellular changes and restore organ function.

Additional Languages

Spanish

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Clinical Divisions

Pediatric Intensive Care Unit PICU

Research Divisions

Critical Care



Blog Posts

Cincinnati Children’s Launches 6 COVID-19 Research Projects

Infectious Diseases and Vaccines

Cincinnati Children’s Launches 6 COVID-19 Research Projects

Steve Standage, MD, Ming Tan, PhD ...5/26/2020

My Education

MD: University of Rochester School of Medicine, Rochester, NY, 2005.

Residency: General Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA, 2008.

Fellowship: Pediatric Critical Care, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2011.

My Publications

Multi-Organ Transcriptome Dynamics in a Mouse Model of Cecal Ligation and Puncture-Induced Polymicrobial Sepsis. Rumienczyk, I; Kulecka, M; Ostrowski, J; Mar, D; Bomsztyk, K; Standage, SW; Mikula, M. Journal of Inflammation Research. 2021; 14:2377-2388.

The application of omic technologies to research in sepsis-associated acute kidney injury. Hasson, D; Goldstein, SL; Standage, SW. Pediatric Nephrology. 2021; 36:1075-1086.

NMR-based serum and urine metabolomic profile reveals suppression of mitochondrial pathways in experimental sepsis-associated acute kidney injury. Standage, SW; Xu, S; Brown, L; Ma, Q; Koterba, A; Lahni, P; Devarajan, P; Kennedy, MA. American Journal of Physiology - Renal Physiology. 2021; 320:F984-F1000.

PPARα contributes to protection against metabolic and inflammatory derangements associated with acute kidney injury in experimental sepsis. Iwaki, T; Bennion, BG; Stensoe, EK; Lynn, JC; Otinga, C; Djukovic, D; Raftery, D; Fei, L; Wong, HR; Liles, WC; et al. Physiological Reports. 2019; 7.

PPARα augments heart function and cardiac fatty acid oxidation in early experimental polymicrobial sepsis. Standage, SW; Bennion, BG; Knowles, TO; Ledee, DR; Portman, MA; McGuire, JK; Liles, WC; Olson, AK. American Journal of Physiology - Heart and Circulatory Physiology. 2017; 312:H239-H249.

Nonhematopoietic Peroxisome Proliferator-Activated Receptor-α Protects Against Cardiac Injury and Enhances Survival in Experimental Polymicrobial Sepsis. Standage, SW; Waworuntu, RL; Delaney, MA; Maskal, SM; Bennion, BG; Duffield, JS; Parks, WC; Liles, WC; McGuire, JK. Critical Care Medicine. 2016; 44:e594-e603.