Health
Researchers link specific proteins to diabetic cardiomyopathy
Researchers at the University of Barcelona in Spain have identified a potential target for the treatment of diabetic patients who develop a serious heart disease called diabetic cardiomyopathy.
In people with cardiomyopathy, the heart has difficulty pumping blood to other parts of the body, which can cause chest pain, shortness of breath, swelling, fatigue, dizziness, and fainting. It can cause heart failure, blood clots, heart valve problems, and cardiac arrest.
People with diabetes are more likely to develop cardiomyopathy. High blood sugar levels caused by diabetes damage blood vessels and increase the likelihood of fat deposits. a study published In September 2024, more than a third of people with type 1 diabetes were found to have diabetic heart disease or diabetic cardiomyopathy.
In a study at the University of Barcelona, published This month it's P.pharmacological researchresearchers explain how activation of a protein called the nuclear receptor PPARδ may have beneficial effects in disease. PPARδ is present in all cells, including skeletal muscle, heart, and liver.
Researchers found that PPARδ proteins are associated with metabolic diseases characterized by inflammation, including insulin resistance, dyslipidemia, and metabolic fatty liver disease induced by obesity and diabetes. They found that activating PPARδ receptors helps slow down inflammatory and fibrotic processes in both animal models and human heart cells under hyperglycemic conditions.
In diabetes and obesity, insulin resistance may cause the heart to obtain energy almost exclusively from mitochondrial oxidation of fatty acids. This causes lipid accumulation within the myocardium, causing lipotoxicity, which causes the myocardium to require more oxygen.
Diabetic hyperglycemia and lipotoxicity cause cardiac inflammation and fibrosis through activation of pro-inflammatory and pro-fibrotic transcription factors (NF-ΛB and AP-1). Once activated, these factors drive the process of cardiac remodeling, increasing myocardial stiffness and preventing the heart from relaxing after contraction.
Activation of NF-ΛB and AP-1, along with mitogen-activated protein kinase (MAPK) activity, induces cell death in cardiomyocytes, which also contributes to contractile dysfunction in diabetic cardiomyopathy.
“All these processes together lead to extracellular cardiac remodeling, systolic dysfunction, left ventricular hypertrophy, dilated cardiomyopathy, and ultimately heart failure,” says Xavier Palomar.
said one of the researchers involved in the study in a news release. Palomar co-led the study with Manuel Vázquez-Carrera. Both are from the Faculty of Pharmacy and Food Sciences of the University of Barcelona, the Institute of Biomedical Sciences of the University of Barcelona, and the Institute of Sant Joan de Deu.
“Inhibiting these MAPKs can prevent inflammation and fibrosis not only in the heart, but also in other organs and tissues in a variety of pathological conditions, such as the liver, lungs, kidneys, and even skeletal muscle,” Vasquez-Carrera said. the doctor said.
Related: FDA grants early approval for rare liver disease drug
A therapy targeting PPARδ received accelerated approval by the FDA in August 2024 to treat patients with primary biliary cholangitis (PBC), a progressive autoimmune disease caused by the destruction of bile ducts in the liver. . Gilead's Libdelgi (Celadelpar) is an oral therapy that can activate PPARδ and reduce bile acids.
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