Diabetes, Heart, and Cardiovascular Diseases News Chronicle.      Article 214

The SGLT2 Inhibitor Canagliflozin, An Anti-diabetes Drug Can Reduce The Risk Of Kidney And Heart Disease

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A study at the George Institute for Global Health, Australia shows that the risk reduction to a number of health issues with the SGLT2 inhibitor canagliflozin (Invokana), an anti-diabetes drug. A trial on more than 10,000 patients from 30 countries with canagliflozin, a type 2 diabetes (T2D) drug shows the following benefits.

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Health Issue The Risk Reduction
Cardiovascular diseases 14%
Hospitalization with heart failure 33%
Progression of serious kidney decline 40%
Reduction in blood pressure (BP)  
Weight loss  

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The SGLT2 inhibitor canagliflozin, an anti-diabetes drug can reduce the risk of kidney and heart disease.

But the risk of amputation (leg, foot or toe) may double with the canagliflozin, an anti-diabetes drug. The reason for the increased risk of amputations with canagliflozin is not known.

The co-author of the study was Vlado Perkovic, M.B., B.S., Ph.D., executive director, The George Institute for Global Health, Australia and Bruce Neal, M.B., Ch.B., Ph.D.

The study was presented at the American Diabetes Association Conference, San Diego and also published in the New England Journal of Medicine. Title of the article is "Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes".
DOI: doi.org/10.1056/NEJMoa1611925

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Canagliflozin: It is a sodium-glucose cotransporter 2 (SGLT2) inhibitors class (or gliflozin class type 2 diabetes) drug. This drug works by blocking the reabsorption of glucose or sugar into the bloodstream, resulting in more glucose or sugar pass out of the body through urine.

The Stem Cell From Damaged Heart Tissue May Worsen Heart Damage


Earlier studies show that the end-stage heart failure patients can be treated with a 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 them.

The stem cell from damaged heart tissue may worsen heart damage.

This procedure can cause the regeneration of blood vessels and heart muscle cells by using the stem cells of the patient. There are two options to extract stem cells from the patient. Either from the heart tissue or from the bone marrow.

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A study at the Tel Aviv University, Israel shows that the stem cell therapy to heart failure patients using cardiac stem cells is more harmful (as the stem cells are sick), can cause inflammation and ineffective. The damaged cardiac stem cells may develop inflammatory properties and can cause further damage to the heart.

The researchers came to the above conclusion after conducting experiments on the mice models. The experimental mice model had a heart attack and the heart attack causes dysfunction of its left ventricular. They extracted stem cells from the cardiac tissue of the mice model. The extracted stem cells are injected back into the mice model to repair damaged heart tissue. They studied the function and remodeling of the heart. The study has found the development of inflammatory condition leading to increased risk of heart damage instead of repairing the damaged heart tissue.

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With this experiment, researchers have concluded that the stem cells collected from the already diseased heart muscle do not help in the healing of their heart after an injury.

In the experiments, the researchers have identified a gene called TLR4, a gene that causes the development of inflammatory properties in the transplanted stem cells of the already diseased heart muscle. The stem cells can be transformed into a reparative state by deleting the TLR4 gene. The researchers believe that this method can be used for autologous stem cell transplant to a patient with heart failure.

The leader of the study was Prof Jonathan Leor, Sackler Faculty of Medicine, Tel Aviv University, Israel. The study was published in the journal Circulation. Title of the article is "Left Ventricular Dysfunction Switches Mesenchymal Stromal Cells Toward an Inflammatory Phenotype and Impairs Their Reparative Properties Via Toll-Like Receptor-4."
DOI: doi.org/10.1161/CIRCULATIONAHA.116.023527

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Published on July 22, 2017


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