Researchers came to this conclusion after conducting trials with canagliflozin, a type 2 diabetes (T2D) drug among more than 10,000 patients in 30 countries. But the risk of amputation (leg, foot or toe) doubles with the canagliflozin type 2 diabetes drug (T2D). Reasons for the increased risk of amputations with canagliflozin are not known.
Co-author of the study was Vlado Perkovic, M.B., B.S., Ph.D., executive director, The George Institute Australia and Bruce Neal, M.B., Ch.B., Ph.D. The study findings were presented at the American Diabetes Association Conference, San Diego and also published in the New England Journal of Medicine, under the title "Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes".
Canagliflozin : A sodium-glucose cotransporter 2 (SGLT2) inhibitors class or gliflozin class type 2 diabetes (T2D) drug. This drug works by blocking reabsorption of glucose or sugar into bloodstream resulting in more glucose or sugar passed out of the body through urine.
Earlier studies shows end-stage heart failure patients can be treated with stem cell therapy as this procedure is a "last resort" treatment for those patients. Autologous stem cell therapy is gaining popularity among end-stage heart failure patients as there is no other treatment available to treat end-stage heart failure condition. This procedure results in the regeneration of blood vessel and heart muscle cells with the usage of patient's own stem cells. There are two options to derive stem cells from the patient, either from heart tissue or from bone marrow.
A study done by researchers from the Tel Aviv University, Israel shows stem cell therapy to heart failure patients involving cardiac stem cells is more harmful (as stem cells were sick), causes inflammation and ineffective than helpful. The damaged cardiac stem cells may develop inflammatory properties and cause further damage to heart. Researchers came to this conclusion after conducting experiments with mice models. The experimental mice model had a heart attack and the heart attack caused dysfunction of its left ventricular. They collected stem cells from the cardiac tissue of the mice. Researchers injected the collected stem cells back into the mice to repair its heart tissue. They studied the heart's function and remodeling. Researchers observed development of inflammatory condition leading to increased risk of heart damage instead of repairing the damaged heart tissue. With this experiment, researchers concluded that stem cells collected from sick hearts do not help in healing of their heart after injury.
In those experiments, researchers identified TLR4, a gene that causes the development of inflammatory properties in the transplanted stem cells of the sick heart. The stem cells can be transformed into a reparative state by deleting TLR4 gene. Researchers believe this method can be used in a patient with heart failure to transform autologous stem cell therapy. The leader of the study was Prof Jonathan Leor, Sackler Faculty of Medicine, Tel Aviv University, Israel. The study findings were published in the journal Circulation.
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Published by Jammi Vasista, Chennai, India.