Efferocytosis And Its Oft-Unstated Role In Artery Clogging.
Atherosclerotic plaques can be "naturally" removed... but how?
The word “efferocytosis” isn’t one that is frequently thrown about these days. Most heart disease patients would not have heard of this word before, because rarely is it (if ever) discussed by their doctors.
Oddly, though, it is a biological process that occurs naturally within our bodies. Much like autophagy, which more people would have heard of:
Of course, before dead cells are destroyed, they have to be programmed to commit suicide first. There’s a marked difference when we have dead skin that sloughs off as compared to flaps of dead skin that we have to cut off when we suffer an injury. Somehow, those flaps of skin still can cause pain, while skin that sloughs off is painless.
Because programmed suicide is easier to deal with than a sudden, accidental death.
It happens in real life too - it’s more about how much control one has over their own fates.
In the realm of programmed suicides, a cell that is programmed to commit suicide undergoes apoptosis.
It is stated in this article that “the human body turns over more than one million cells per second through a process known as programmed cell death (PrCD), or apoptosis”.
That article goes on further to state that “the body engages in an evolutionarily conserved process known as programmed cell removal (PrCR), or efferocytosis” to remove those dead cells.
And we can see this process occurring in atherosclerotic plaques, too.
These plaques contain a necrotic core that is rich in dead apoptotic cells.
And unfortunately, if all these dead cells aren’t cleared in time, they will contribute to the development of a pro-inflammatory environment.
Of course, this pro-inflammatory environment significantly affects the cells that are requisite for conducting efferocytosis.
The cells that are requisite for conducting efferocytosis? The immune system’s macrophages, of course.
They are generally present as 2 different phenotypes: the M1 and the M2 variants.
This article suggests that a macrophage is initially neutral, but it polarises into the M1 or M2 phenotype based on the prevailing cytokine signal. The pro-inflammatory cytokine tumour necrosis factor alpha (TNF-α), for instance, promotes M1 polarisation.
And it is also known that “increased concentrations of TNF-α are found in acute and chronic inflammatory conditions”, as reported in this article.
So when we experience an injury, for instance, we will experience a bout of acute inflammation around the injured region - this inflammation will trigger a preferential differentiation of new macrophage cells into the M1 variant to conduct phagocytosis on the injured/dead muscle cells and clear out cellular debris.
When their job is done, they hand over the next set of duties for the M2 macrophages to conduct, and that is when the inflammatory signal intensity will subside. When the M1 guys have not completed their end of the work, the inflammation signal ought to remain, and with it any associated symptoms of pain, aches and/or swelling.
But let’s get back to the topic of heart disease.
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