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Top Stories - Cardiovascular Pathobiology

Dr. Towler will join Sanford-Burnham as professor and director of the Cardiovascular Pathobiology Program
Dwight Towler to lead...

Dwight A. Towler, M.D., Ph.D., will join Sanford-Burnham at Lake Nona as professor and director of...

Dr. Towler (left) with his team of scientists at his Lake Nona lab.
Hard at work against the...

Sanford-Burnham researchers identified a potential drug target to prevent the hardening of arteries...

Researchers in the Bodmer lab have discovered a new pathway to fat-related heart disease.
A different path to...

Fruit fly study demonstrates how lipotoxic cardiomyopathy might occur in genetically obese...

Calorie-burning brown fat (shown here) gets a boost from natriuretic peptides in the heart
Heart hormone helps shape fat...

Dr. Sheila Collins and colleagues discover that the pathway to losing fat is heavily influenced by a...

Hard at work against the hardening of arteries

by Bruce Lieberman on May 16, 2013 at 1:00 pm | 0 Comments
Full Article
Dr. Towler (left) with his team of scientists at his Lake Nona lab.

Dr. Towler (left) with his team of scientists at his Lake Nona lab.

The hardening of arteries is a hallmark of atherosclerosis, an often deadly disease in which plaques, excessive connective tissue, and other changes build up inside vessel walls and squeeze off the flow of oxygen-rich blood throughout the body. Now, researchers at our Diabetes and Obesity Research Center have described the molecular and cellular pathway that leads to this hardening of the arteries—and zeroed in on a particularly destructive protein called Dkk1.

Their study was published online today by Arteriosclerosis, Thrombosis, and Vascular Biology. The findings suggest that the development of drug therapies to selectively inhibit endothelial Dkk1 signaling may help limit arteriosclerotic disease.

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Diabetic fruit flies support buzz about dietary sugar dangers

by Heather Buschman, Ph.D. on January 17, 2013 at 5:33 am | 1 comment
Full Article
Cardiac fibrosis (shown in purple), a hallmark of heart disease, is clearly increased in fruit flies on a high-sugar diet (right), as compared to flies on a normal diet (left).

Cardiac fibrosis (shown in purple), a hallmark of heart disease, is clearly increased in fruit flies on a high-sugar diet (right), as compared to flies on a normal diet (left).

First fruit fly model of diet-induced type 2 diabetes shows how high-sugar diet affects the heart and reveals new therapeutic opportunities

Regularly consuming sucrose—the type of sugar found in many sweetened beverages—increases a person’s risk of heart disease. In a study published January 10 in the journal PLOS Genetics, researchers at Sanford-Burnham Medical Research Institute and Mount Sinai School of Medicine used fruit flies, a well-established model for human health and disease, to determine exactly how sucrose affects heart function. In addition, the researchers discovered that blocking this cellular mechanism prevents sucrose-related heart problems.

“Our study reveals a number of specific sugar-processing enzymes that could be targeted with therapies aimed at reducing sucrose’s unhealthy effects on the heart,” said Karen Ocorr, Ph.D., research assistant professor at Sanford-Burnham and the study’s corresponding author.

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Sanford-Burnham research projects selected to go to space

by Communications Staff on November 29, 2012 at 6:30 am | 1 comment
Full Article
The International Space Station, as seen from the departing Space Shuttle Discovery in 2009 (Image courtesy of NASA)

The International Space Station, as seen from the departing Space Shuttle Discovery in 2009 (Image courtesy of NASA)

Space Florida to send two experiments from Sanford-Burnham Medical Research Institute to the International Space Station

We’re excited to announce today that two of our research teams have won Space Florida’s International Space Station (ISS) Research Competition. Eight teams were selected from a pool of international applicants to send experiments to space in late 2013. The competition was initiated by Space Florida, the state’s spaceport and aerospace authority, and NanoRacks, LLC. Sanford-Burnham’s research will fly as payloads to the ISS aboard a SpaceX Falcon 9 launch vehicle and research will be conducted on board the U.S. National Lab at the ISS.

Here’s what the two teams are hoping to accomplish:

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Dwight Towler to lead Sanford-Burnham’s Cardiovascular Pathobiology Program

by Patrick Bartosch on October 17, 2012 at 5:15 am | 0 Comments
Full Article
Dr. Towler will join Sanford-Burnham as professor and director of the Cardiovascular Pathobiology Program

Dr. Towler will join Sanford-Burnham as professor and director of the Cardiovascular Pathobiology Program

We’re pleased to announce that Dwight A. Towler, M.D., Ph.D. is joining Sanford-Burnham’s Lake Nona, Orlando campus as professor and director of our Cardiovascular Pathobiology Program. As program director, Towler will lead the Institute’s research into fundamental and early translational aspects of cardiovascular biology, physiology, and disease. Before joining Sanford-Burnham, Towler was the Ira M. Lang Professor of Medicine in the Division of Endocrinology, Metabolism, and Lipid Research at Washington University in St. Louis, Mo. He will formally assume the position at Sanford-Burnham in November 2012.

“We’re thrilled to welcome Dr. Towler, a world-renowned endocrinologist and vascular biologist, to the Institute,” said Sanford-Burnham at Lake Nona scientific director Daniel Kelly, M.D. “At Washington University, Dr. Towler conducted extensive research into the cardiovascular effects of type 2 diabetes, which is a key research area within the Diabetes and Obesity Research Center at Sanford-Burnham.”

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Meet Rebecca, Sanford-Burnham employee and obesity study participant

by Patrick Bartosch on August 3, 2012 at 5:57 am | 0 Comments
Full Article
Scientists at the TRI measure Rebecca Kaercher's oxygen levels, among other parameters

Scientists at the TRI measure Rebecca Kaercher's oxygen levels, among other parameters

Rebecca Kaercher has been struggling with her weight for years. “Losing weight has been a very frustrating endeavor for me. I go on diets, I work out, but I just don’t lose any weight,” she says. Rebecca has been working at Sanford-Burnham at Lake Nona for three years and, together with a few of her Institute coworkers, was thrilled to volunteer as a metabolism and weight loss study subject at the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes (TRI). “I am very proud to work at Sanford-Burnham and I want to be an active part of our research. Except for being overweight, I am a very healthy person. I don’t have high cholesterol, no high blood pressure, no diabetes. So it was hard for me to understand why I didn’t lose any weight.”

Rebecca is the kind of person scientists at the TRI are currently looking for as volunteers – people who have tried to lose weight by exercising and changing their diets but didn’t succeed. As with many other people who have the same problem, something in Rebecca’s body keeps her from losing weight and researchers at the TRI are trying to find out what that could be. The common perception is that overweight people only need to eat healthier and exercise more in order to lose weight. But this simple approach does not work for everyone. That is about to change with the research taking place at the TRI’s new facility in downtown Orlando.

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A “twisted” grand opening ceremony

by Patrick Bartosch on March 29, 2012 at 3:35 pm | 0 Comments
Full Article
TRI grand opening speakers (from left to right): John Reed, Terry Owen, Dan Kelly, Steve Smith, Lars Houmann, Des Cummings, Don Jernigan

TRI grand opening speakers (from left to right): John Reed, Terry Owen, Dan Kelly, Steve Smith, Lars Houmann, Des Cummings, Don Jernigan

“My goal is to cure diabetes,” Steven Smith, M.D., scientific director of the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes (TRI), said boldly at the opening ceremony of the TRI’s new state-of-the-art facility in downtown Orlando on March 27. “We believe that personalized medicine is our best shot at discovering cures for our most serious health problems like diabetes.”

The ceremony’s highlight was the unveiling of a spectacular nine-foot double-helix DNA structure that will be placed at the main entrance of the building, symbolizing the fundamental research being conducted at the TRI, as well as the synergies and collaborations the TRI represents. Selected board members and presenters each added one illuminated “bar,” representing a nucleotide, to the double helix.

“This is one of those rare times when the reality far exceeds the dream,” said John Reed, M.D., Ph.D., CEO of Sanford-Burnham. “The TRI is a wonderful opportunity for our organization, which will bring more and more to life our slogan From Research, the Power to Cure. We’re very excited about this opportunity to take our relationship with Florida Hospital to the next level.”

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Heart hormone helps shape fat metabolism

by Bruce Lieberman on February 6, 2012 at 9:01 am | 2 Comments
Full Article
Calorie-burning brown fat (shown here) gets a boost from natriuretic peptides in the heart

Calorie-burning brown fat (shown here) gets a boost from natriuretic peptides in the heart

It’s well known that exercising reduces body weight because it draws on fat stores that muscle can burn as fuel. But a new study at Sanford-Burnham suggests that the heart also plays a role in breaking down fat. In their study, published February 6 in the Journal of Clinical Investigation, Sheila Collins, Ph.D. and colleagues detail how hormones released by the heart stimulate fat cell metabolism. These hormones turn on a molecular mechanism similar to what’s activated when the body is exposed to cold and burns fat to generate heat. This study adds another dimension to our understanding of how the body regulates fat tissue and may someday lead to new ways to manipulate the process with drugs to reduce weight in obese patients or maintain it in individuals who experience pathological weight loss during chronic heart failure.

“Exercise is always going to raise your blood pressure some, so there’s the potential that these heart hormones—called cardiac natriuretic peptides—are being released and contributing to the breakdown of fats,” said Collins, professor in the Diabetes and Obesity Research Center at Sanford-Burnham’s Lake Nona campus in Orlando and senior author of the study. “Over a period of time, natriuretic peptides could also be leading to an increase in the numbers of brown fat cells, which we know are very important for protection against diet-induced obesity, at least in laboratory experiments.”

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Research highlights: American Heart Association Scientific Sessions 2011

by Deborah Robison on November 25, 2011 at 6:32 am | 0 Comments
Full Article
Drs. Daniel Kelly (left) and Ola Martin

Drs. Daniel Kelly (left) and Ola Martin

Several Sanford-Burnham investigators presented their research findings at the American Heart Association (AHA) Scientific Sessions 2011 on November 13-16, where more than 14,000 clinicians and researchers gathered in Orlando, Florida.

During his lecture at the Cardiovascular Seminar Series, Dr. Daniel Kelly, scientific director of Sanford-Burnham’s Lake Nona facility in Orlando, presented his laboratory’s ongoing work to determine the role of “energy starvation” in the development of heart failure. The Kelly laboratory has found that mitochondria, the cell’s energy-generating machines, becomes dysfunctional during the development of heart failure caused by common disease states such as high blood pressure and heart attacks. Dr. Kelly also presented several strategies his laboratory is pursuing to identify new drug targets to replenish mitochondria in the failing heart, including using the power of proteomics (defining the levels of all proteins operating in a cell) and metabolomics (identifying all the body’s metabolites).

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New therapeutic target for heart disease

by Heather Buschman, Ph.D. on November 17, 2011 at 11:34 am | 0 Comments
Full Article
Hyungsoo Kim, Ph.D., postdoctoral researcher and first author of the study

Mitochondria are often called cellular “powerhouses” because they convert nutrients into energy. But these tiny structures also help determine cellular lifespan. Scientists are now discovering how mitochondria alternate between duplicating and fragmenting and how these events help cells adapt to diverse physiological conditions.

In a paper published November 18 in Molecular Cell, a team led by Dr. Ze’ev Ronai discovered that the protein Siah2 regulates mitochondrial fragmentation under low oxygen conditions. The significance of these findings is demonstrated by the heart’s response to oxygen shortage and ischemia, the tissue damage caused by lack of oxygen, when the researchers inhibited Siah2. In cells and mice lacking the protein, heart cell death was prevented. As a result, tissue damage was reduced in a mouse model that mimics a heart attack.

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CARing for pulmonary arterial hypertension

by Heather Buschman, Ph.D. on July 22, 2011 at 9:57 am | 0 Comments
Full Article
Dr. Masanobu Komatsu

Dr. Masanobu Komatsu

Pulmonary arteries carry blood from the heart to the lungs, where they pick up fresh oxygen for distribution to the rest of the body. Since almost every cell in the human body needs oxygen in order to convert nutrients into energy, pulmonary artery function is crucial. Pulmonary arterial hypertension (PAH) occurs when pressure builds up in these blood vessels, impairing this function. People with PAH experience shortness of breath, fatigue and chest pain. As the condition worsens, the heart has to work harder and harder to pump blood, sometimes leading to heart failure.

Despite eight approved clinical therapies for PAH and additional therapies currently in trials, there is no cure. What’s more, current treatments don’t specifically target pulmonary arteries, which can lead to severe side effects.

Sanford-Burnham scientists, led by Drs. Masanobu Komatsu and Dr. Takeo Urakami, in collaboration with VBS Pharmaceuticals, recently discovered a peptide (a short protein) that selectively targets and penetrates lung blood vessels affected by PAH. When the team tested this peptide, called CARSKNKDC (or CAR for short) in a rodent model of PAH, it homed in on hypertensive lungs, but spared healthy lungs and other organs. CAR also accumulated in other regions of the respiratory system that play crucial roles in PAH development and progression.

Published in the June 2011 issue of the American Journal of Pathology, these findings indicate that CAR could be used to deliver therapeutic compounds and imaging probes directly to PAH lungs.

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Recycled: Close to the heart

by Heather Buschman, Ph.D. on July 14, 2011 at 11:59 am | 0 Comments
Full Article
Heather & Avery

the author and her daughter

Editor’s note: We originally ran this post last summer and it quickly became one of our most popular. In honor of my mother’s birthday, July 14, I’d like to share it with you again (with an updated picture!).

Early one morning eleven years ago, I was visiting some friends while enjoying a break from college, when my dad called to tell me that my mom had died. It was sudden and completely unexpected. She was only 46 years old, healthy and seemingly full of life. My mom just went to work one evening (alone on the late shift) and never came home. As my dad tried to explain to me at the time, she just collapsed and that was it – nobody else was there to know what really happened. It was devastating to me and my family and our lives were forever changed. Not only was she gone, but we never had much of an explanation as to why. What caused her death and could it have been prevented? This was one of the hardest parts for me as both a daughter and as a young scientist. I read the medical examiner’s report myself. It wasn’t a heart attack and it wasn’t a stroke. The cause of death was simply listed as “heart failure.”

That still frustrates me. As I’ve pointed out to countless people in the years since, with all we know about the human body, it’s surprising that cause of death can still be a mystery. “Heart failure” just seems like a catch-all phrase – an easy thing to say when there’s no other explanation. After all, isn’t that what kills us all in the end?

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Personalized Medicine 101

by Amelia Tomas on April 21, 2011 at 3:54 pm | 1 comment
Full Article
Dr. Steven Smith, Scientific Director for the Florida Hospital Sanford-Burnham Translational Research Institute, demonstrates sophisticated equipment used in metabolic studies.

Dr. Steven Smith, Scientific Director for the Florida Hospital Sanford-Burnham Translational Research Institute, cares for a patient.

In 2003, the completion of the human genome project gave us an unprecedented amount of genetic information. From this, a new clinical concept is emerging: personalized medicine.

Conventional medical care generalizes treatment to all patients with a particular disease. But since a disease is as individual as the person who has it, casting a wide therapeutic net has its limitations. For one, patients with a certain genetic makeup might not respond to a particular drug as well as patients with different genetics, or they might experience different side effects. As personalized medicine becomes a reality, it could rectify these less-than-ideal situations.

From the diagnostic point-of-view, personalized medicine is a shift from reactive to proactive. Based on a person’s health, genetic, and environmental profiles, doctors practicing personalized medicine could assess a patient’s risk for acquiring a genetic disease before any symptoms develop. This might allow them to target the specific genes that account for illness (the BRCA1/BRCA2 genes that predispose a woman to breast cancer, for example), incorporate a prevention strategy, and monitor those genes over time. When it comes to treatment, personalized drugs could be prescribed based on an individual’s molecular “build” and targeting treatment where it will do the most good and the least harm.

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Targeting Arterial Plaque

by Josh Baxt on April 19, 2011 at 4:00 am | 1 comment
Full Article
Dr. Erkki Ruoslahti

Dr. Erkki Ruoslahti

Atherosclerotic plaque is the fatty material that builds up on arterial walls, where it can lead to heart disease and stroke. Atherosclerosis is currently treated with dietary changes, angioplasty (which uses a balloon to move the plaque aside) or more invasive procedures. Using drugs to break up these fatty plaques would be an enticing alternative, but delivery poses a problem. How do we precisely target the therapeutic agent to the diseased areas, leaving healthy tissues unaffected?

Dr. Erkki Ruoslahti and colleagues at Sanford-Burnham and UC Santa Barbara may have found a solution. For many years, Dr. Ruoslahti has been using specially designed peptides (pieces of proteins) to target cancer and other diseases. In a paper published online on April 11 by the Proceedings of the National Academy of Sciences, the Ruoslahti lab reports the discovery of a new peptide that can guide drugs or imaging agents specifically to atherosclerotic plaques.

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Blog Your Heart Out!

by Heather Buschman, Ph.D. on February 11, 2011 at 3:01 pm | 1 comment
Full Article

February is American Heart Month and today we are joining the American Heart Association and Fitlosophy, Inc. for the 2nd annual Blog Your Heart Out Day! Here we share some of our favorite blog posts on heart disease, the leading cause of death for both men and women…

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A different path to fat-related heart disease

by Heather Buschman, Ph.D. on January 18, 2011 at 3:09 pm | 2 Comments
Full Article

Heart disease is the leading cause of death for both men and women in the United States. But heart disease is more than just one disease; there are many different ‘flavors’ that can result from a heart attack, high blood pressure, diabetes or other causes. In lipotoxic cardiomyopathy, for example, heart function is disrupted by fat accumulation in heart cells. Obesity and high-fat diets are major risk factors for lipotoxic cardiomyopathy, but scientists recently unraveled an alternative pathway to lipotoxic cardiomyopathy in fruit flies – a genetic mechanism that occurs independently of a diet high in fat. Their study lays the foundation for the development of new ways to combat lipotoxic cardiomyopathy and other types of heart disease.

“It’s a well-accepted notion that if you eat too much fatty food and your body can’t metabolize it properly, you can become obese and this can lead to lipotoxic cardiomyopathy. Our study shows that there is also an alternative cause of obesity and associated heart problems – an imbalance in the fats that normally make up the basic structure of our cells,” explained Dr. Hui-Ying Lim, post-doctoral researcher and lead author of the study.

In this study, the researchers analyzed mutant fruit flies (called easily shocked mutants) that have abnormally low levels of phosphatidylethanolamine (PE), a type of fat that makes up a major component of cellular membranes in both flies and mammals. They found that these flies compensate for low PE levels by initiating a mechanism for synthesizing fat. In this mechanism, a protein called sterol regulatory element-binding protein (SREBP) turns on genes encoding metabolic enzymes that synthesize more fat.

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