Wedoany.com Report on Feb 7th, Approximately 64 million people worldwide suffer from heart failure. Due to a lack of effective treatments to halt disease progression, nearly half of patients die within five years of diagnosis. Heart failure occurs when the heart's pumping capacity drops below 40%. Most existing treatments focus on reducing the workload on the heart rather than targeting the root cause of the disease. Researchers are still exploring the causes of heart failure and the mechanisms behind its worsening.
Recent research suggests the immune system may be a key factor in the worsening of heart failure. T cells, part of the body's defense mechanism, normally help the body recover from injury and fight infection. They promote wound healing by producing anti-inflammatory cytokines and regulate other immune cells to combat pathogens.
However, when T cells become abnormally activated and attack the body's own tissues, they can trigger autoimmune diseases. For instance, type 1 diabetes and psoriasis are both linked to mistaken attacks by T cells. Research over the past 13 years indicates that the behavior of T cells during heart failure warrants attention.
If T cells can help heal skin wounds, why can't they repair heart damage? Through mouse experiments, a research team found that a type of immune cell called helper T cells produces pro-inflammatory cytokines. These proteins cause additional damage to the heart during heart failure, leading to sustained worsening of the condition.
In the latest human tissue study, scientists analyzed samples of failing hearts obtained from transplant patients. The results showed that T cells remain active in these heart tissues and continuously activate pro-inflammatory proteins, exacerbating heart damage rather than promoting repair. The protein composition within T cells from failing hearts shares characteristics similar to T cells found in autoimmune diseases.
These findings suggest that heart failure may induce T cells to exhibit a response pattern akin to that seen in autoimmune diseases. Although the specific mechanisms of heart failure still require further elucidation, viewing it as an immune-related disorder offers new avenues for treatment. Targeting overactive T cells could become a potential strategy to halt the progression of heart failure and improve patient outcomes.
