Engineering a Healthier Heart: Noor Momin Receives AHA Transformational Project Award

When someone survives a heart attack, the battle isn’t always over. In fact, nearly one-third of survivors go on to develop heart failure—a progressive weakening of the heart muscle that affects millions and contributes to roughly 500,000 deaths in the U.S. each year.

Dr. Noor Momin, the Stephenson Foundation Term Assistant Professor of Innovation in Bioengineering at Penn, is working to change that. Her lab’s innovative approach to immune modulation after heart attacks has just been recognized with the prestigious American Heart Association (AHA) Transformational Project Award for 2025. This award supports groundbreaking ideas that hold the potential to significantlya dvance cardiovascular and cerebrovascular research. (See award criteria.)

(Photo Credit: Mark Griffey, Penn Engineering)

A Targeted Strategy to Prevent Heart Failure

Following a heart attack, the immune system springs into action to repair damaged tissue. But when that response lingers or becomes excessive, it can cause additional harm—like a repair crew overstaying its welcome and inadvertently worsening the damage.

Momin’s lab is developing a targeted strategy using cytokines to control this immune response. Cytokines are used by immune cells to communicate with each other and other cells. Instead of delivering just a cytokine, which can lead to harmful side effects in healthy tissues, they’ve re-engineered it to home to damaged heart tissue. Early preclinical tests have shown that this approach can prevent heart failure with minimal side effects. 

The lab is now focused on conducting further dose and treatment schedule optimization, safety and mechanistic studies to move the technology towards clinical translation.

This line of research could lead to a fundamentally new way to prevent heart failure in heart attack survivors, directly supporting the American Heart Association’s mission to help people live longer, healthier lives.

From Seed to Solution: The Role of CPE4H

This transformative research began with a spark: seed funding from the Penn Center for Precision Engineering for Health (CPE4H).

“The seed grant was crucial for getting our project off the ground right after we moved to One uCity in the summer of 2024,” Momin explains. “Having those funds immediately available allowed us to start research without delay and maintain momentum in gathering preliminary data. This work directly led to securing AHA funding in under a year – which is exceptionally fast for translational research. The seed grant essentially jump started everything. We’re really grateful for that support.”

That rapid trajectory is exactly what the CPE4H aims to support.

“Noor’s success with the American Heart Association proposal is very exciting to me and the center,” says Daniel A. Hammer, Inaugural Director of CPE4H and the Alfred G. and Meta A. Ennis Professor for Bioengineering and Chemical and Biomolecular Engineering. “Noor’s work embodies the principles of the CPE4H – using engineering principles to develop therapies that have real consequences for human health, in this case cardiovascular disease. In addition, it’s particularly gratifying that we can support and initiate funding for an Assistant Professor who is at the early stages of her career.”

Engineering Innovation, Saving Lives

As Dr. Momin’s project progresses, it offers a glimpse into a future where heart attack survivors have better tools to prevent the onset of heart failure—tools born from innovative thinking and catalyzed by early support.

Engineering a Healthier Future: Kelsey Swingle’s Journey from Penn to Rice

Precision medicine. Women’s health. RNA therapeutics. Kelsey Swingle’s next chapter advances science that can’t wait.

On July 1, Kelsey Swingle, Ph.D., officially joined Rice University as an Assistant Professor in Bioengineering, a remarkable leap directly from doctoral training to a tenure track faculty position. She’s not just launching a lab, she’s continuing a mission shaped at the University of Pennsylvania’s Center for Precision Engineering for Health (CPE4H).

The new paper’s lead author Kelsey Swingle (GrEng’27) at work in the lab. (Credit: Kevin Monko)

At CPE4H Swingle’s research pioneered new ways to deliver mRNA therapeutics using lipid nanoparticles, with applications that go as far as treating deadly pregnancy complications like pre-eclampsia.

“Kelsey’s unique application is to use these technologies to treat specific diseases, such as to target the placenta during pregnancy,” said Daniel A. Hammer, Inaugural Director of CPE4H. “Her work is a wonderful combination of precise molecular delivery applied to a real problem in human health.”

In a world where reproductive health remains chronically underfunded and underserved, Swingle’s research targets a profound gap. Her innovations hold promise for early intervention in pregnancy disorders, pushing the boundaries of what medicine can treat and when.

Kelsey was trained in Michael Mitchell’s lab at Penn Bioengineering.

“Mike has continuously guided and supported me, and gave me the unique opportunity to launch a new research area in the Mitchell Lab focused on women’s health,” Swingle said.

But her impact extended far beyond science. Swingle played a pivotal role in Penn’s translational research community, through platforms like the CPE4H Focus Friday seminars and cross-lab collaboration in the UCity space, environments designed to accelerate innovation at the intersection of engineering and medicine.

“I’ve found that one of the biggest challenges during graduate school is the opportunity to wear multiple hats—as a student, researcher, scientist, mentee, mentor, friend, and role model—which can feel really overwhelming and daunting, especially in the beginning. I clearly remember sharing these feelings with Mike during the second year of my Ph.D., and he encouraged me to focus on executing good science and being a team player, and to have confidence everything else would work itself out,” Swigle shared. “Now that I’ve accepted a faculty position, everything has worked out even better than I could have anticipated.”

“Kelsey is the complete scholar. She is extremely hard working and creative in her research, and is always looking for new areas to grow and challenge herself. But she is also an incredible teacher and mentor of the next generation. It is rare to start an independent faculty position right after completing a PhD, but Kelsey is absolutely ready for it and will hit the ground running,” observed Michael Mitchell, Associate Professor for Penn Bioengineering.

Research team from left to right includes Kelsey Swingle, Hannah Safford, Alex Hamilton, Ajay Thatte, Hannah Geisler, and Mike Mitchell. (Credit: Penn Engineering)

Now, at Rice, Swingle will launch the Swingle Lab, carrying forward a research agenda that sits at the interface of biomaterials, immune engineering, and reproductive biology. The stakes? Future therapies for complex and under-treated conditions — with global impact.

“I’m a big believer that cutting-edge research takes a team of great people that are eager to work together,” Swingle said. “I’m excited to explore opportunities to collaborate and learn from everyone in Rice Bioengineering and the broader scientific community at the Texas Medical Center in Houston.”

For Penn, Swingle’s story reaffirms its mission to train the next generation of engineers not only to innovate, but to lead.

“Because Kelsey will, in turn, train students and postdoctoral associates in her own laboratory, her career has an important, multiplicative effect on the influence of the center broadly across the scientific community,” Hammer emphasized.

“Kelsey has done an incredible job here at Penn Bioengineering, CPE4H, and the Mitchell Lab. I’m very hopeful that her faculty position at top-10 ranked Rice Bioengineering will enable her to make important contributions to the fields of drug delivery and women’s health, ” shared Mitchell.

Kelsey Swingle is more than a rising star. She’s a catalyst, proving what happens when the right minds are given the creative freedom, mentorship, and mission to engineer a more equitable and personalized future for healthcare.

Penn Engineers Turn Toxic Fungus into Anti-Cancer Drug

by Ian Scheffler

First author Qiuyue Nie and coauthor Maria Zotova, from left, purify samples of the fungus. (Credit: Bella Ciervo)

Penn-led researchers have turned a deadly fungus into a potent cancer-fighting compound. After isolating a new class of molecules from Aspergillus flavus, a toxic crop fungus linked to deaths in the excavations of ancient tombs, the researchers modified the chemicals and tested them against leukemia cells. The result? A promising cancer-killing compound that rivals FDA-approved drugs and opens up new frontiers in the discovery of more fungal medicines.

“Fungi gave us penicillin,” says Sherry Gao, Presidential Penn Compact Associate Professor in Chemical and Biomolecular Engineering (CBE) and in Bioengineering (BE) and senior author of a new paper in Nature Chemical Biology on the findings. “These results show that many more medicines derived from natural products remain to be found.”

From Curse to Cure

A. flavus, named for its yellow spores, has long been a microbial villain. After archaeologists opened King Tutankhamun’s tomb in the 1920s, a series of untimely deaths among the excavation team fueled rumors of a pharaoh’s curse. Decades later, doctors theorized that fungal spores, dormant for millennia, could have played a role.

A sample of Aspergillus flavus cultured in the Gao Lab. (Credit: Bella Ciervo)

In the 1970s, a dozen scientists entered the tomb of Casimir IV in Poland. Within weeks, 10 of them died. Later investigations revealed the tomb contained A. flavus, whose toxins can lead to lung infections, especially in people with compromised immune systems.

Now, that same fungus is the unlikely source of a promising new cancer therapy.

Read the full story in Penn Engineering Today.

Researchers crack the code of body’s ancient immune defense

by Nathi Magubane & Ian Scheffler

(Left) Pre-ignition (below the activation threshold) Only a handful of immune “tags” (C3b proteins) cover the nanoparticle, so it barely sticks to the white membrane—too few contact points means the immune cell simply can’t grab on. (Right) Post-ignition (above the activation threshold). The nanoparticle is now densely coated with C3b tags, and the immune-cell membrane reaches out with many matching receptors. Dozens of little “hooks” latch on at once, creating a strong, multivalent grip that pulls the particle in for engulfment.(Image: Ravi Radhakrishnan)

How does your body distinguish friendly visitors, like medications and medical devices, from dangerous invaders such as viruses and other infectious agents? The answer lies in a protein network dating back half a billion years—before humans diverged from sea urchins, notes Jake Brenner, a physician-scientist at the University of Pennsylvania.

“The complement system is perhaps the oldest-known part of our extracellular immune system,” says Brenner. “It plays a crucial role in identifying foreign materials like microbes, medical devices, or new drugs—particularly the larger ones like in the COVID vaccine.”

The complement system can, however, simultaneously play friend and foe, offering protection with one hand while backhanding the body with the other. In some cases, this ancient network can significantly exacerbate conditions like stroke by targeting the body’s own tissues. As Brenner explains, leaking blood vessels allow complement proteins to target brain tissue, causing the immune system to mistakenly launch an attack on the body’s own cells and worsen patient outcomes.

Now, using a combination of wet-lab experimentation, coupled differential equations, and computational-based modeling and simulations, an interdisciplinary team from the School of Engineering and Applied Science and the Perelman School of Medicine has decrypted the mathematical language behind the complement network’s “decision” to attack.

Reporting their findings in Cell, the team identifies a molecular tipping point known as the critical percolation threshold, which is based on how densely complement-binding sites are spaced on the surfaces of the model invader they engineered. If spacing between binding sites is too wide—landing above a threshold—complement activation fizzles out; below it, complement network ignites, a chain reaction of immune agent recruitment which spreads like wildfire.

Read the full story in Penn Today.

Optogenetic Functional Profiling Indicates New Mechanisms of Drug Tolerance in Cancer Cells

While modern cancer treatments can have tremendous therapeutic impact, formidable obstacles remain. Foremost among these is drug resistance, the ability of cancers to withstand and ultimately progress despite the presence of an anti-cancer drug. However, ongoing research provides hope that these challenges can be overcome, including recent work performed by Penn Engineers.

The lab of Lukasz J. Bugaj, Assistant Professor in the Department of Bioengineering, recently published an article that uncovers new mechanisms of how oncogenes interact  with important pathways of cellular signaling that are associated with resistance. This work, titled “Oncogenic EML4-ALK Assemblies Suppress Growth Factor Perception and Modulate Drug Tolerance,” applied a new technique called ‘optogenetic functional profiling’ that allowed measurement of how important molecular signaling pathways respond to precise perturbations applied by the researchers.  By applying this technique to many different cell types, the group found important differences in resistance-associated signaling between cancer cells and healthy cells 

Specifically, the research showed that an oncogene called EML4-ALK, which activates oncogenic signaling, simultaneously inactivates adjacent pathways that can cause resistance.  As a consequence, once an oncogene-blocking drug is applied, the inactivation is relieved, thus boosting activity through these adjacent, resistance-associated pathways.  The study also showed that these pathways were not only de-repressed, but were actively stimulated by neighboring cancer cells, further enhancing cell survival in the presence of the drug. 

“Our work shows that oncogenes, while driving cell division in cancer cells, simultaneously suppress the cells’ regulation by their environment,” said Dr. Bugaj. “While the work reveals mechanisms of paradoxical responses to drug treatment related to resistance, they may also inspire new ideas for therapies that can more efficiently kill cancer cells while maintaining suppression of resistance signaling. This work was co-led by PhD student David Gonzalez-Martinez and by Lee Roth, PhD, a postdoctoral fellow, and was supported by a grant from the American Cancer Society. 

Dr. Bugaj’s article can be read here.

Loebel Lab Arrives in 2025

Reliance Industries Term Assistant Professor Claudia Loebel will establish her lab at The University of Pennsylvania’s Department of Bioengineering and the Center for Precision Engineering for Health in January 2025.

Dr. Loebel received her MD from Martin Luther University Halle Wittenberg, Germany and her Ph.D from ETH Zurich, Switzerland.

“My laboratory is developing testable models to investigate how extracellular signals regulate cellular function to direct the development and regeneration of organs, ultimately leading to more effective therapeutic treatments,” said Dr. Loebel in her research statement. “Building upon my K99/R00 and American Lung Association Innovation Awards, a major focus of my group has been on understanding the role of mechanical forces across various states of pulmonary development and regeneration.”

Dr. Loebel’s team is formed with an exciting combination of interdisciplinary scholars including postdoctoral associates, graduate and undergraduate students whose philosophy encourages respect for people’s differences, acknowledging and honoring religious and cultural practices, and foster diverse thinking. Dr. Loebel is also a recent recipient of the 2025 Rising Star Award from BMES CMBE, and also won the CMBE Young Innovators award for her published article, “Magnetoactive, Kirigami- Inspired Hammoks to Probe Lung Epithelial Cell Function.”

The Loebel Lab is funded by the David and Lucile Packard Foundation Fellowship, whose mission is dedicated to further the advancement of people and communities with their three overreaching and interdependent goals: building societies, protecting and restoring the natural world, and investing in families.

New Class of Encrypted Peptides Offer Hope in Fight Against Antibiotic Resistance

by Eric Horvath

Cesar de la Fuente, Presidential Assistant Professor with appointments in the Perelman School of Medicine, School of Engineering and School of Arts & Sciences (Image: Eric Sucar)

In a significant advance against the growing threat of antibiotic-resistant bacteria, researchers have identified a novel class of antimicrobial agents known as encrypted peptides, which may expand the immune system’s arsenal of tools to fight infection. The findings, published in Trends in Biotechnology by Cell Press, reveal that many antimicrobial molecules originate from proteins not traditionally associated with immune responses.

Unlike conventional antibiotics that target specific bacterial processes, these newly discovered peptides disrupt the protective membranes surrounding bacterial cells. By inserting themselves into these membranes—much like breaching a fortress wall—the peptides destabilize and ultimately destroy the bacteria.

“Our findings suggest that these previously overlooked molecules could be key players in the immune system’s response to infection,” says César de la Fuente, presidential assistant professor in bioengineering and in chemical and biomolecular engineering in the School of Engineering and Applied Science, in psychiatry and microbiology in the Perelman School of Medicine, and in chemistry in the School of Arts & Sciences, who led the research team. “This may not only redefine how we understand immunity but also opens up new possibilities for treating drug-resistant infections.”

Read the full story in Penn Medicine News.

Developing Kidneys from Scratch: Alex Hughes Tackles the Tremendous Burden of Kidney Disease

by Ian Scheffler

Alex Hughes, Assistant Professor in Bioengineering, holds a model of a developing kidney. (Credit: Bella Ciervo)

To Alex Hughes, Assistant Professor in Bioengineering within Penn Engineering and in Cell and Developmental Biology within Penn Medicine, the kidney is a work of art. “I find the development of the kidney to be a really beautiful process,” says Hughes.

Most people only ever see the organ in cross-section, through textbooks or by dissecting animal kidneys in high school biology class: a bean-shaped slice with lots of tiny tubes. “I think that really undersells how amazing the structure is,” says Hughes, who points out that kidneys grow in utero like forests of pipes, branching exponentially.

Densely packed with tubules clustered in units known as nephrons, kidneys cleanse the blood, maintaining the body’s fluid and electrolyte balance, while also regulating blood pressure. The organ played a crucial role in vertebrates emerging from the ocean: as one paper puts it, kidneys preserve the primordial ocean in all of us.

Unfortunately, kidneys struggle in the modern world. Excessively salty food, being overweight, not exercising enough, drinking too much and smoking can all raise blood pressure, which damages the kidney’s tiny blood vessels, as does diabetes.

In some cases, damage to the kidney’s nephrons can be slowed with lifestyle changes, but, unlike the liver, bones and skin, which can regrow damaged tissue, kidneys have a limited capacity to regenerate. At present, without a transplant, the nephrons we have at birth must last a lifetime.

Read the full story in Penn Engineering Today.

Studying Wikipedia Browsing Habits to Learn How People Learn

by Nathi Magubane

A hyperlink network from English Wikipedia, with only 0.1% of articles (nodes) and their connections (edges) visualized. Seven different reader journeys through this network are highlighted in various colors. The network is organized by topic and displayed using a layout that groups related articles together. (Image: Dale Zhou)

At one point or another, you may have gone online looking for a specific bit of information and found yourself  “going down the Wiki rabbit hole” as you discover wholly new, ever-more fascinating related topics — some trivial, some relevant — and you may have gone so far down the hole it’s difficult to piece together what brought you there to begin with.

According to the University of Pennsylvania’s Dani Bassett, who recently worked with a collaborative team of researcher to examine the browsing habits of 482,760 Wikipedia readers from 50 different countries, this style of information acquisition is called the “busybody.” This is someone who goes from one idea or piece of information to another, and the two pieces may not relate to each other much.

“The busybody loves any and all kinds of newness, they’re happy to jump from here to there, with seemingly no rhyme or reason, and this is contrasted by the ‘hunter,’ which is a more goal-oriented, focused person who seeks to solve a problem, find a missing factor, or fill out a model of the world,” says Bassett.

In the research, published in the journal Science Advances, Bassett and colleagues discovered stark differences in browsing habits between countries with more education and gender equality versus less equality, raising key questions about the impact of culture on curiosity and learning.

Read the full story in Penn Today.

Dani S. Bassett is the J. Peter Skirkanich Professor at the University of Pennsylvania with a primary appointment in the School of Engineering and Applied Science’s Department of Bioengineering and secondary appointments in the School of Arts & Sciences’ Department of Physics & Astronomy, Penn Engineering’s Department of Electrical and Systems Engineering, and the Perelman School of Medicine’s Departments of Neurology and Psychiatry.

Penn’s Siloxane-Enhanced Nanoparticles Chart a New Path in Precision mRNA MedicineBeyond Displays: Liquid Crystals in Motion Mimic Biological Systems

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By adjusting the chemical structure of lipid nanoparticles (LNPs), Penn Engineers have discovered how to target specific organs, a major breakthrough in precision medicine. (Love Employee via Getty Images)

Penn Engineers have discovered a novel means of directing lipid nanoparticles (LNPs), the revolutionary molecules that delivered the COVID-19 vaccines, to target specific tissues, presaging a new era in personalized medicine and gene therapy.

While past research — including at Penn Engineering — has screened “libraries” of LNPs to find specific variants that target organs like the lungs, this approach is akin to trial and error. “We’ve never understood how the structure of one key component of the LNP, the ionizable lipid, determines the ultimate destination of LNPs to organs beyond the liver,” says Michael J. Mitchell, Associate Professor in Bioengineering.

In a new paper published in Nature Nanotechnology, Mitchell’s group describes how subtle adjustments to the chemical structure of the ionizable lipid, a key component of the LNP, allows for tissue-specific delivery, in particular to the liver, lungs and spleen.

Read the full story in Penn Engineering Today.