By Amanda Ashley, Sr. Director of Research & Innovation Communications
Every day, people arrive at hospitals with blocked arteries — from heart attacks, strokes, or traumatic injuries. The medical response has become a national standard: restore blood flow as fast as possible, a goal measured from the time the patient arrives in the emergency room to the moment a balloon tipped catheter opens their blocked heart artery as “door-to-balloon time.”
Thanks to decades of scientific progress, that time has dropped dramatically. Lives are being saved every hour because of it.
What Happens During Ischemia-Reperfusion Injury (IRI)?
When blood flow stops, cells enter survival mode. Oxygen drops. The body conserves energy.
When blood flow returns, mitochondria — the “engines” of the cell — are suddenly flooded with oxygen. They struggle to process it and instead produce toxic reactive oxygen species (ROS). This leads to:
- Inflammation
- Electrical instability in the heart
- Cellular stress and tissue damage
- Long-term impacts like heart failure
This happens in:
- Heart attacks (PCI procedures)
- Strokes (tPA or thrombectomy)
- Trauma surgery
- Kidney, liver, or heart transplants — often deciding graft success or failure
Today, there is no approved therapy to prevent ischemia-reperfusion injury
But what happens after the artery opens? That is where medicine still faces an unanswered challenge. The University of Utah is demonstrating that this challenge can be addressed, and faster than many thought possible.
The lifesaving procedure can also cause harm.
When oxygen-starved tissue suddenly receives new blood flow, a paradox occurs: the cells can become overwhelmed and damaged. This is called ischemia-reperfusion injury (IRI), a biological consequence of restoring blood flow.
It happens in:
- Emergency rooms
- Cardiac catheterization labs
- Vascular operating rooms
- Transplant operating rooms
- Stroke treatments and trauma care
- Every district in the country
“We know how to save someone from blockage. But what happens after the artery opens? That’s an unanswered problem in modern medicine.” — Dr. Robin Shaw
A Large-Scale Problem — With a Human Cost
- 805,000 heart attacks in the U.S. every year
- 500,000–600,000 patients receive reperfusion procedures — directly exposing them to IRI
- Up to 50% of heart damage can occur after the artery is opened
- Stroke, transplant, trauma — all share this same cellular challenge
- No therapy exists to prevent it
- IRI market projected to reach $1.5B by 2033, but it represents something far bigger: lives shaped by damage we know how to prevent
“This isn’t a niche issue. It affects families across America.” — Dr. Shaw
A Proven Working Model; Built in Utah
The University of Utah has built a functioning pathway to confront this problem, not as a hypothesis, but in practice. What began as a research challenge has become a working model that moves science faster from the lab to patient care. And importantly, it is structured to be replicable at other public universities across the country.
This is not theory, it is proof of concept.
One Scientist Asking Different Questions
At the University of Utah, one of the researchers confronting this challenge is Dr. Robin M. Shaw, MD, PhD, a cardiologist, scientist, and system-builder who has spent his career studying how heart cells behave under stress, and how science can better serve patients.

His work spans cardiac muscle biology, mitochondrial function, and translational approaches to treating heart failure and ischemic injury. He serves as Director of the Nora Eccles Harrison Cardiovascular Research & Training Institute (CVRTI) and holds both the Nora Eccles Harrison Presidential Endowed Chair and a professorship in Internal Medicine.
“What good is discovery if it can’t reach the people who need it? says Dr. Shaw. That question has guided both his research and the infrastructure he has built: a pathway that connects basic discovery all the way to patient care, not someday, but now.
The Research Continuum — How Science Becomes Solutions
University research is not a single step — it is a living continuum. Every stage depends on the one before it.
| Stage | Purpose | Key Question | Example at U |
| Discovery | Understand biological mechanisms | How does life work? | Fundamental cardiac cell & mitochondrial research (individual Rutter, Selzman and Shaw Laboratories) |
| Validation | Test mechanisms & feasibility | Is it real? | Small animal IRI studies in individual laboratories |
| Translation | Move toward clinical viability | Will it work in people? | Physiologically appropriate large animal models + regulatory prep (ASAP) |
| Implementation | Deliver therapy to patients | Can it help people? | FDA submission → clinical trials → standard of care |
“My dream isn’t just to discover something, it’s to see that discovery help a patient. That’s the full journey of science.” — Dr. Shaw
A Utah Case Study — The Model in Motion
At the University of Utah, researchers, clinicians, and translational experts have built something uncommon: a working system that moves discoveries toward the FDA pathway faster and more cost-effectively than industry.
Within the Nora Eccles Harrison Cardiovascular Research & Training Institute (CVRTI), a cross-unit team built what is often missing nationwide:
- Operating rooms ready for translational science
- Regulatory expertise in house
- Large animal models for efficacy testing
- Clinical trial design capacity
- Interdisciplinary collaboration, without the silos
This is the foundation of the ASAP Project (American Science Acceleration Project), three University-originated therapies targeting ischemia reperfusion injury, all tested side-by-side in a 12-month translational sprint:
| Therapy | Origin | Stage | Pathway |
| GJA1-20k | Shaw Lab | Small animal IRI data complete | Pre-IND preparation underway |
| VB253 | Rutter Lab / Vettore Biosciences | Safety in humans established for other indications, need pre-clinical efficacy for IRI indications | Could advance directly to clinical trial if there is pre-clinical IRI efficacy |
| hAF | Selzman Lab | Small animal IRI data complete, safety in humans established for other indications | Pre-IND preparation underway |
By taking advantage of existing University of Utah infrastructure and collaborations, the total projected cost is under $1 million and projected time is one year— not $10–$20M and multiple years to advance three separate preclinical candidates. That represents a new model for translational infrastructure.
“This isn’t about speed for speed’s sake. It’s about moving fast enough to matter to people whose lives are on the line.” Erin Rothwell, Vice President for Research at the University of Utah.
A Moment for National Consideration
The question is no longer whether universities can move science forward.
It’s whether we will resource them to scale what already works.
If the U.S. wants to compete globally in biotech and health innovation, research universities are not just laboratories. They are national infrastructure. “Universities generate the ideas. The question now is: can we carry these ideas forward to the bedside? What we’re establishing is, yes, we can.”— Dr. Shaw
A Model Other Universities Can Build
What makes this effort different is not just the therapies, but the structure behind them.
What has been developed at CVRTI is not proprietary, it’s portable. It does not depend on a single building or a single scientist. It depends on aligned incentives, flexible research infrastructure, and leadership willing to connect the work across disciplines.
The University of Utah is demonstrating that a public research institution, with the right systems in place, can move science from bench to bedside faster than the traditional biotech model.
This is not a one-time success. It is proof of concept. What has worked here can work elsewhere. Not as a copy, but as a blueprint. The question now is not whether universities can do this. The question is how many will and how many lives could be changed if they do.