Metabolic Stress and Immune System Interactions Make Heart Failure a Result

Metabolic Stress and Immune System Interactions Make Heart Failure a Result ...

According to a review article from UTSouthwestern researchers and colleagues, the dominant form of heart failure worldwide appears to be the result of a strong, bidirectional interaction between the body''s response to metabolic stress and the immune system.

According to the articles, heart failure with a preserved ejection fraction affects millions of people around the world, but we currently have little to offer these patients because the mechanisms behind it have been unknown. We now have a clue into this condition that we didn''t have even five years ago, as well as observations that might lead to viable clinical objectives.

Heart failure with reduced ejection fraction (HFrEF), in which the amount of blood that leaves the heart with each beat decreases, and heart failure with preserved ejection fraction (HFpEF), in which the heart is unable to fill with blood to capacity. While HFrEF has long been the most common form, it has overtaken HFrEF as the most common form.

HFrEF may be improved with different methods, but these approaches are likely to adversely affect the HFpEF, according to Dr. Hill, a topic his lab has studied for years. Despite the fact that weight loss is a problem that many individuals struggle with, leading him to require treatment.

In this paper, Hill and his colleagues outline findings from the past several years that indicate joint metabolic and immune dysfunction as the root cause of HFpEF. For example, fat tissue secretes inflammatory molecules that migrate to the heart, repurposing immune cells evident in heart biopsy samples from individuals with HFpEF. At the same time, heart toxicity caused by overutilization of fatty acids as fuel in metabolic syndrome appears to stimulate an immune response, leading to a vicious cycle.

Crosstalk between fat tissue, the immune system, and the heart appears to increase both immune and metabolic stress, causing the heart to fail over time. However, what this crosstalk occurs, how it affects, and how to prevent them, remain unclear. HFpEF patients will undergo additional research, according to Dr. Hill.

Dr. Hill said research from our laboratory and others is exploring the possibility of therapeutic goals that must be investigated. There''s a good chance that we might have therapies available for this untreated condition within the next decade.

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