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As society ages, the number of patients suffering from heart failure increases significantly. Fibrosis, or excessive growth of fibrotic tissue in the heart, is associated with the progression of heart failure. A group from the Nagoya University Graduate School of Medicine in Japan has discovered an enzyme called protein kinase N (PKN) that regulates heart fibrosis.
This enzyme transforms cardiac fibroblasts into myofibroblasts, which compromises the integrity of the heart. Removing this enzyme reduces ventricular dysfunction, indicating that anti-PKN therapy is a potential therapy to protect patients from heart failure.
These findings were published in Nature Communications.
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Risk of heart attack
The heart maintains its integrity using small cells called fibroblasts, which often transform into myofibroblasts after damage. Myofibroblasts promote wound healing by forming fibrous connective tissue such as collagen and elastin. However, in heart failure patients, they often collect excess tissue, resulting in stiffening and reduced function of the heart tissue, known as fibrosis. This process reduces the integrity of the heart’s structure, increasing the risk of heart attack.
The enzyme PKN is involved in the signaling cascade that causes cardiac fibroblast activation. A group led by Dr. Satoya Yoshida, Mikito Takefuji and Toyoaki Murohara at the Department of Cardiology, Nagoya University Graduate School of Medicine, suspected the involvement of PKN in the transformation of fibroblasts into myofibroblasts seen in fibrosis. Together with colleagues from the Max Planck Institute, they investigated its role.
In mammalian cells, there are three forms of PKN: PKN1, 2, and 3. Using RNA-sequencing data, they identified PKN1 and 2 in cardiac fibroblasts. The study used mice raised without PKN1 and PKN2. It was found that although heart function remained unaffected, there was a significant decrease in actin and collagen expression in myocardial infarction and heart failure models. These proteins are essential components responsible for the tissue formation seen in fibrosis. They also found that mice with suppressed PKN1 and 2 did not convert fibroblasts into myofibroblasts.
“Although our study was performed in a mouse model, PKN expression has been demonstrated in human heart fibroblasts, so similar results are expected in human trials,” said Dr. Yoshida. “In fact, almost all heart diseases are closely related to cardiac fibrosis. I believe our findings contribute to improving the diagnosis of many heart diseases, especially heart failure.”
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