Thus the venom of a spider will help us limit the damage after a heart attack

Thus the venom of a spider will help us limit the damage after a heart attack

Hi1: behind this acronym there could be a solution to reduce the risk of chronic damage linked to heart attack, especially after reperfusion. This process defines the potential problems that characterize the recovery of the blood supply after a phase of ischemia that has damaged myocardial cells or neurons, following a heart attack or a cerebral stroke.

The molecule, studied by a team from the University of Queensland, was identified in the venom of a particular funnel web spider, which is part of a family of arachnids of different species. At the moment, we are only at the beginning of the trials and it will take time to use this treatment strategy on humans.

But, as reported by research conducted on animals by experts at the University of Queensland and presented on European Heart Journal (first name Meredith A. Redd), however, important prospects are opened up for preserving the cardiac tissue and neurons that are faced with the phases immediately following the resumption of blood circulation in the area affected by ischemia. Always remembering that early aid and treatment is essential to protect the heart after cardiac ischemia. Arriving early can save your life!

Possible cardioprotective effect

At the moment, it must be said, protecting the heart after a heart attack is one of the most complex challenges for medicine. The experts, on an animal model, tested the action of the spider venom protein on a specific target, the acid-sensitive ion channel 1a (ASIC1a). Inhibiting its action could in fact protect the brain and heart from damage related to ischemia, even if the mechanism through which this process occurs is not known.

The researchers, testing the effect of Hi1a’s action, saw that in the models treated with this substance deriving from spider venom, the size of the infarct lesion was reduced 24 hours after the experimentally induced ischemia. Above all, over time, this treatment has made it possible to limit the risk of the appearance of myocardial dysfunction which in some way paves the way to heart failure.

The research, in some way, confirms what has already been observed by a study coordinated by Nathan Palpant And Glenn King from the Institute of Molecular Biosciences of the Australian university (also among the authors of the research we are talking about), who had shown how Hi1a could protect cells from damage caused by heart attack and stroke.

The treatment appears safe

As reported in a note from the University of Queensland itself, the research appears really interesting for possible future developments, which still remain to be evaluated. We are still in the preclinical testing phase, in fact. But according to Palpant, “these tests represent an important step in helping us understand how Hi1a could work in therapy, in which phase of the heart attack it could be used and at what doses.”

But it’s not enough. The research, on the efficacy front, seems to demonstrate the possibility of filling a “gap” of treatments for cardiovascular protection in the early stages after a heart attack, given that a single drug used in this sense, after having almost finished its clinical trials, it was abandoned due to side effects.

However, Australian experts point out an interesting aspect on this front: Hi1a would only interact with cells in the affected area ischemia and therefore damaged, without having any action (at least up to this point of the experiments) on the healthy areas of the myocardium. Which would reduce the possibility of side effects. It must be said that it is certainly not the first time that effective solutions have been sought for the treatment of human diseases starting from the potentially lethal venom of an animal. The venom of the viper, for example, was one of the bases of the treatments that a few decades ago made it possible to arrive at thrombolysis, or the “dissolution” of the blood clot that blocks circulation in a coronary artery, allowing better treatment of the heart attack and stroke in emergency.

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