Within
the initial cell of a new multicellular organism lies a set of directives that
will not only steer its descendants through cycles of growth, development, and
reproduction, but also toward the inevitable conclusion of life. As a facet of
this intricate program, numerous cells follow a path of self-termination once
they have fulfilled their designated purpose. This process, termed apoptosis
(derived from the Greek word for "dropping off" or "falling
off"), is initiated by molecular cues that trigger the activation of
internally stored self-destruct mechanisms. These mechanisms, akin to
stockpiled weaponry, include enzymes specialized in cleaving proteins.
Visualize these enzymes as folded pocket knives that, once unfolded, sever
structural proteins, including the foundational elements of cytoskeletons and
the nucleosomes that arrange DNA.
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| Ultrastructural features of cell death by apoptosis |
The
dying cells undergo a sequence of shrinking, condensation, and eventual
fragmentation, culminating in the release of small membrane-bound apoptotic
bodies. These bodies are typically engulfed and cleared by other cells through
a process known as phagocytosis. Importantly, this mode of cell death prevents
the uncontrolled release of intracellular components into the extracellular
environment, a safeguard against potential harmful effects. In stark contrast,
cell death resulting from tissue damage, referred to as necrosis, leads to cell
swelling and rupture. This, in turn, releases intracellular contents that can
inflict harm on neighboring cells and trigger inflammation.
