Substance From Magnolia Tree Can Protect From Cardiac Hypertrophy

Substance From Magnolia Tree Can Protect From Cardiac Hypertrophy

A recent study published in the online journal Nature Communications reported that a natural compound be found in the magnolia tree has the potential to offer protection against heart hypertrophy — a condition related to the thickening of cardiac muscle frequently caused by chronic high blood pressure that can lead to heart failure.

Researchers found that if injected into mice, honokiol (hoh-NOH’-kee-ohl) could reduce the excess growth of each cardiac muscle cell and decreased ventricular wall thickness, and also prevent the assembly of interstitial fibrosis — the constraint of cardiac muscle cells resulting in the reduction of their capacity to contract. Researchers also found evidence of the capacity to protect heart muscle cells from the damage that results from the oxidative stress that can damage DNA and provoke mutations.

The research team reported how this substance manages to protect the heart; scientists found that the compound activates a protein linked to stress resistance, delayed aging and metabolic regulation.

“Honokiol, by increasing SIRT3 levels, effectively blocked both the induction and progression of cardiac hypertrophy in mice. It even mitigated pre-existing cardiac hypertrophy. This has the potential to play a significant role in the prevention and treatment of heart failure,” said study author Dr. Mahesh Gupta.

He continued, “to the best of our knowledge, this is the first report to describe a pharmacologic activator of SIRT3. Until now, caloric restriction combined with endurance exercise has been the only way to boost SIRT3 levels. Very few people have been able to follow such a rigorous regimen.”

SIRT3 is active in mitochondria (responsible for energy production within the cells) and plays a crucial role in energy metabolism, becoming extremely important in preventing acetylation that can alter the way proteins function. When SIRT3 is not present, mitochondrial proteins are hyperacetylated and their function might be compromised.

Studies in humans have evidenced that sedentary patients older than 60 years of age have about 40 percent less SIRT3. While studying mice without the SIRT3 gene, researchers found they have lower levels of ATP (40% lower) when compared to animals who carry the gene (ATP is the main source of cellular energy).

Scientists found that honokiol lowered mitochondrial protein acetylation and activated SIRT3. They confirmed that this activation could prevent hypertrophy and block the production of fibroblasts without causing any visible toxicity.

The authors said this could be “a potential therapeutic strategy to prevent adverse cardiac remodeling and other diseases associated with abnormal cellular growth and organ fibrosis.”

“We treated the mice with injections into the peritoneal cavity rather than by mouth, which is how this compound has traditionally been administered. We are testing to see if oral use will have a similar effect.” Despite that, “we are tremendously excited. We are working to design a clinical trial involving patients with cardiac hypertrophy and potentially other metabolic diseases, such as type 2 diabetes,” Dr. Gupta added.

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