This new molecule could help improve heart attack recovery
Researchers have developed a new molecule that could help preserve heart tissue during, and even after, a heart attack.
Cardiologists say that when a heart attack occurs, time is muscle, said a researcher.
Without oxygen supplied by blood flow, heart cells die- fast. But while a heart attack may only reduce blood and oxygen to an isolated section of heart cells- causing what's called hypoxic-ischemic injury- those dying cells send signals to their neighbours.
The problem is that the area of dying tissue is not quarantined. Damaged heart cells start to send out signals to otherwise healthy cells, and the injury becomes much bigger, said the researcher.
Scientists sometimes call this spread of injury signals to nearby healthy tissues a bystander effect. But what if there were a way to keep the injury localized to the group of cells that are directly affected by the hypoxic-ischemic injury while allowing the nearby muscle cells to remain intact.
Nearly a decade ago, a researcher stumbled across a promising discovery. The team discovered a compound that targets the activity of channels in cell membranes responsible for controlling key aspects of the bystander effect.
But the compound, called alphaCT1, also had other unexpected and beneficial effects, particularly in relation to skin wound healing.
We found that it helped reduce inflammation, helped heal chronic wounds such as diabetic foot ulcers, he said.
The group designed molecules with slight chemical differences from the parent molecule, which led to an unexpected discovery. One of the alphaCT1 variants- called alpha CT11- showed more potency than the parent molecule.
AlphaCT11 seems to be even more effective than the original peptide in protecting hearts from an ischemic injury similar to those occurring during a heart attack, he said.
The study revealed that alphaCT11 gives a robust injury-reducing effect, even when given 20 minutes after the loss of blood flow that causes ischemic injury. When put to the same test, the parent peptide did not appear to provide a heart-protective effect when administered after ischemic injury.
aplhaCT11 could provide the basis for a new way to treat heart attacks and prevent the spread of damage that occurs immediately after a heart attack, he said.
The researchers perfused isolated laboratory mouse hearts, keeping the organ alive and beating for a number of hours. Ongoing studies, through collaboration with others, will examine how alphaCT11 performs in live mice.
The researcher is also developing new methods for delivering alphaCT11 using naturally-derived tiny lipid droplets called exosomes. These newer experiments could provide a stepping stone toward clinical trials in patients who have suffered a heart attack.
Cardiologists say that when a heart attack occurs, time is muscle, said a researcher.
Without oxygen supplied by blood flow, heart cells die- fast. But while a heart attack may only reduce blood and oxygen to an isolated section of heart cells- causing what's called hypoxic-ischemic injury- those dying cells send signals to their neighbours.
The problem is that the area of dying tissue is not quarantined. Damaged heart cells start to send out signals to otherwise healthy cells, and the injury becomes much bigger, said the researcher.
Scientists sometimes call this spread of injury signals to nearby healthy tissues a bystander effect. But what if there were a way to keep the injury localized to the group of cells that are directly affected by the hypoxic-ischemic injury while allowing the nearby muscle cells to remain intact.
Nearly a decade ago, a researcher stumbled across a promising discovery. The team discovered a compound that targets the activity of channels in cell membranes responsible for controlling key aspects of the bystander effect.
But the compound, called alphaCT1, also had other unexpected and beneficial effects, particularly in relation to skin wound healing.
We found that it helped reduce inflammation, helped heal chronic wounds such as diabetic foot ulcers, he said.
The group designed molecules with slight chemical differences from the parent molecule, which led to an unexpected discovery. One of the alphaCT1 variants- called alpha CT11- showed more potency than the parent molecule.
AlphaCT11 seems to be even more effective than the original peptide in protecting hearts from an ischemic injury similar to those occurring during a heart attack, he said.
The study revealed that alphaCT11 gives a robust injury-reducing effect, even when given 20 minutes after the loss of blood flow that causes ischemic injury. When put to the same test, the parent peptide did not appear to provide a heart-protective effect when administered after ischemic injury.
aplhaCT11 could provide the basis for a new way to treat heart attacks and prevent the spread of damage that occurs immediately after a heart attack, he said.
The researchers perfused isolated laboratory mouse hearts, keeping the organ alive and beating for a number of hours. Ongoing studies, through collaboration with others, will examine how alphaCT11 performs in live mice.
The researcher is also developing new methods for delivering alphaCT11 using naturally-derived tiny lipid droplets called exosomes. These newer experiments could provide a stepping stone toward clinical trials in patients who have suffered a heart attack.
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Labels: alphaCT1, blood/ oxygen, cell membranes, diabetic foot ulcers, die fast, during / after, heart attack, heart tissue, isolated section of heart, new molecule, oxygen, preserve, reduce, responsible, wound healing
posted by G S Iyer at 9:54 AM
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