BU Plastic and Reconstructive Surgeon Daniel Roh Receives Emerging Leader Award for Research in Aging
BU’s Daniel Roh will use his National Institute on Aging award to advance work to “improve the delayed wound healing of aging.” Photo courtesy of Roh
BU Plastic and Reconstructive Surgeon Daniel Roh Receives Emerging Leader Award for Research in Aging
National Institute on Aging award includes a five-year, $1.2 million grant for study of wound healing
Aging creeps up on us all, from a few wrinkles here and there to aches in places you never knew could ache. But there are plenty of changes happening on a more fundamental level too. As we age, some cells begin to behave abnormally, for example—they stop dividing and refuse to die. These “zombie cells” can cause inflammation and slow our bodies’ natural healing abilities. Why does this happen? Can we help the body better repair itself by taking out these zombie cells? Or can the cells somehow be used for good?
Daniel Roh, a Boston University Chobanian & Avedisian School of Medicine assistant professor of surgery, has long been fascinated by these questions. He’s been awarded a Paul B. Beeson Emerging Leaders Career Development Award in Aging for his research on wound healing and cellular senescence—the state where a cell deteriorates with age and its functional aspects change. Millions of older Americans are affected by delayed wound healing, which can increase the likelihood of infection and chronic pain.
The award, from the National Institutes of Health’s National Institute on Aging, includes a five-year, $1.2 million research grant. Roh is also a plastic and reconstructive surgeon at Boston Medical Center, BU’s primary teaching hospital.
The Brink spoke with Roh about senescence, his motivation, and how the award will help advance his research.
Q&A
With Daniel Roh
The Brink: What is senescence? Why does it matter?
Roh: When cells and tissues and organs in our body get so much damage, either from aging or from some sort of trauma or radiation, they go into this state of irreversible cell cycle arrest, so these cells cannot proliferate anymore like they’re supposed to. They begin to behave very differently. These cells will stick around and actually resist dying even though they’re abnormal. They produce different types of proteins that cause a lot of inflammation.
Senescence has always had this negative connotation. What I’m interested in is the flip side of senescence: we’re just now beginning to understand that some of these cells—although they stop proliferating and can’t die—can still provide beneficial effects for wound healing and tissue repair.
When you do have these beneficial senescent cells in wound healing, they’re typically only 2 to 5 percent of the total cell population in that wound. So, there are not a lot of these cells, but they serve incredible functions. If you remove them, you prevent healing from happening at a regular rate. We know, based on some data in the lab, that this beneficial wound senescence tends to be more robust in young individuals.
Senescence has always had this negative connotation. What I’m interested in is the flip side of senescence: we’re just now beginning to understand that some of these cells—although they stop proliferating and can’t die—can still provide beneficial effects for wound healing and tissue repair.
The Brink: What are the current treatment programs for dealing with the negative effects of senescence?
In general, senescent cells want to live and they prevent themselves from dying by up-regulating specific pathways. Existing drugs have been able to target some of these pathways so that senescent cells die. A lot of these therapies are called senolytics.
What’s remarkable is that the data from senolytics in mice has shown that if you remove these senescent cells, you can improve physical function with aging and prevent age-related diseases, from Alzheimer’s disease to osteoarthritis. The data has been so robust that now there are actually a handful of these drugs in human clinical trials.
The Brink: What knowledge gaps are you hoping to fill with your research?
What we’re focused on now is identifying what these [beneficial senescent] cells are, what their identity is, what function they have that makes them different, and how they influence the tissue and other cells that are around them. Current drugs don’t target every senescent cell; they target specific types. We need to know what types are good so we don’t target them.
The second aspect that the lab has been looking at is determining what these bad cells are—the chronic senescent cells, so-called zombie cells. We have some interesting data that suggest that if you remove some of these zombie-like cells from each tissue, you can promote a better regenerative environment.
With this information, can we actually improve the delayed wound healing of aging by replacing these senescent cells or some of the factors that they secrete to get these aged individuals to heal faster?
The Brink: What made you want to pursue these research questions?
I’ve always had this question. It’s always been in the back of my mind, every patient and every case I do. What is going on at the cellular level to influence this patient healing faster or taking a longer time to heal? Now, as a BU faculty member, I feel incredibly grateful to have the opportunity to answer these questions that have been burning in my mind during my years of plastic surgery residency training.
A concern that a lot of folks have is that some of these senescent cells actually help in certain situations when we need wound healing and we need tissue repair. So, if you’re treating folks with these senescence-removing agents, how are you actually impacting some of the beneficial roles?
The Brink: What motivates you in your research and practice?
Every day, I see patients, young and old, who are impacted by delayed wound healing in some aspect. I feel incredibly lucky to be able to see the problem in the clinic and in the operating room, think about ways that I can investigate what’s going on at either the cellular or the tissue level, and test those hypotheses in my lab. And then, hopefully, the goal is to bring this back to the patient to improve the quality of their care. Having that motivation makes everything I do that much more meaningful and valuable.
Comments & Discussion
Boston University moderates comments to facilitate an informed, substantive, civil conversation. Abusive, profane, self-promotional, misleading, incoherent or off-topic comments will be rejected. Moderators are staffed during regular business hours (EST) and can only accept comments written in English. Statistics or facts must include a citation or a link to the citation.