A matricellular protein called CCN5 has been found to reverse established cardiac fibrosis - the abnormal thickening of the heart valves, which progresses to heart failure.
Cardiac fibrosis occurs when healthy cardiac cells are replaced with fibrous connective tissue, causing scarring and a stiffer and less compliant cardiac muscle. It is found to be an independent predictor for the progression of heart failure, which accounts for approximately 450,000 deaths per year in the United States. While there currently are no effective cardiac fibrosis therapies available, it is considered a valid target for treatment.
Heart-Rate-Lowering Drug Reduces Risk Of Heart Failure
A heart rate reduction medication can also reduce the risk of diastolic heart failure and cardiac fibrosis, according to a new study.
Advertisement
‘Cardiac fibrosis induced in experimental animal models were treated with CCN5.The key protein was found to reverse the condition.
’
Tweet it Now
The study was led by Roger J. Hajjar, MD, Professor of Medicine and Director of the Cardiovascular Research Center at the Icahn School of Medicine at Mount Sinai, and Woo Jin Park, PhD, Professor of Life Sciences at the Gwangju Institute of Science and Technology (GIST), South Korea.
"Our research is the first to demonstrate the ability to reverse cardiac fibrosis in heart failure models by targeting a specific gene," said Dr. Hajjar. "These findings demonstrate that CCN5 may provide a novel platform for the development of targeted anti-cardiac fibrosis therapies, which could benefit many patients with previously untreatable heart failure. At our Cardiovascular Research Center, we are dedicated to making significant strides in developing potential bench-to-bedside treatments for heart failure and other cardiovascular diseases."
![Pioneering Discovery Could Lead to Preventive Treatment for Sudden Cardiac Death]( "Pioneering Discovery Could Lead to Preventive Treatment for Sudden Cardiac Death")
Now, a team of scientists has used some of David Warshaw's earlier findings to develop a possible treatment to prevent hypertrophic cardiomyopathy (HCM).
Here, Dr. Hajjar and his team, having already established that CCN5 is significantly lower in the myocardium of patients with severe heart failure, examined whether CCN5 can reverse cardiac fibrosis in experimental models. They induced extensive cardiac fibrosis in experimental animal models of heart failure, and then proceeded to transfer CCN5 to the hearts. Eight weeks later, the team examined the cellular and molecular effects.
The results revealed that CCN5 reversed cardiac fibrosis in the models. Researchers used trichrome staining and analysis of myofibroblast contents before and after CCN5 gene transfer to clearly show the reversal. Collectively, these data demonstrate that CCN5 could potentially be used for the development of new anti-cardiac fibrosis therapies.
"Since CCN5 is a secreted protein, we may be able to deliver the CCN5 protein itself rather than the CCN5 gene in the form of recombinant virus or stem cells that are engineered to express CCN5. The efficacy of these alternative approaches has yet to be tested, but they certainly deserve serious consideration," said Dr. Park.
The therapeutic efficacy of CCN5 continues to be investigated in pre-clinical models of heart failure with extensive fibrosis.
This study funded by grants from the NIH and the Korean Government was published online today in the Journal of American College of Cardiology (JACC).
Source: Newswise
Pioneering Discovery Could Lead to Preventive Treatment for Sudden Cardiac Death
Now, a team of scientists has used some of David Warshaw's earlier findings to develop a possible treatment to prevent hypertrophic cardiomyopathy (HCM).
Advertisement
Here, Dr. Hajjar and his team, having already established that CCN5 is significantly lower in the myocardium of patients with severe heart failure, examined whether CCN5 can reverse cardiac fibrosis in experimental models. They induced extensive cardiac fibrosis in experimental animal models of heart failure, and then proceeded to transfer CCN5 to the hearts. Eight weeks later, the team examined the cellular and molecular effects.
The results revealed that CCN5 reversed cardiac fibrosis in the models. Researchers used trichrome staining and analysis of myofibroblast contents before and after CCN5 gene transfer to clearly show the reversal. Collectively, these data demonstrate that CCN5 could potentially be used for the development of new anti-cardiac fibrosis therapies.
"Since CCN5 is a secreted protein, we may be able to deliver the CCN5 protein itself rather than the CCN5 gene in the form of recombinant virus or stem cells that are engineered to express CCN5. The efficacy of these alternative approaches has yet to be tested, but they certainly deserve serious consideration," said Dr. Park.
The therapeutic efficacy of CCN5 continues to be investigated in pre-clinical models of heart failure with extensive fibrosis.
This study funded by grants from the NIH and the Korean Government was published online today in the Journal of American College of Cardiology (JACC).
Source: Newswise
7 Important Measures to Reduce Heart Failure Risk
A new study published in the journal Circulation: Heart Failure has come up with seven most important measures that people can use to rate their heart health.
Advertisement
 Link Between Heart Failure and Red Meat, DiscoveredRed meat contains L-carnitine which is broken down to trimethylamine N-oxide (TMAO), a metabolite, found in heart failure patients. | Advertisement
|
Advertisement
Recommended Reading
Latest Heart Disease News
An association between asymptomatic, CT angiography-detected coronary artery disease and increased heart attack risk identified.
Supervised exercise therapy is safe for people living with one of the most common types of heart failure, known as heart failure with preserved ejection fraction (HFpEF).
Watch out: Cardiac arrest may cause anxiety and depression in women even after four months.
Both cigarettes and smokeless tobacco, a non-combustible form of tobacco exposure are associated with an increased risk of developing peripheral artery disease.
Researchers uncovered an association between heart disease and chronic kidney disease.