Karyorrhexis

In necrosis, however, this step fails to progress in an orderly manner, leaving behind fragmented cellular debris, further contributing to tissue damage and inflammation.

[3] In the intrinsic pathway of apoptosis, environmental factors such as oxidative stress signal pro-apoptotic members of the Bcl-2 protein family to eventually break the outer membrane of the mitochondria.

[5] In the process of karyorrhexis through apoptosis, DNA is fragmented in an orderly manner by endonucleases such as caspase-activated DNase and discrete nucleosomal units are formed.

The fragmented chromatin observed during karyorrhexis is made when activated endonucleases cleave the DNA in between the histones, resulting in orderly, discrete nucleosomal units.

Unlike apoptosis, necrosis cells are characterized by having a ruptured plasma membrane, no association with the activation of caspases, and typically invoking an inflammatory response.

[3] Because necrosis is a caspase-independent process, the nucleus may stay intact during early stages of cell death before being ripped open due to osmotic stress and other factors associated with having a hole in the plasma membrane.

DNA damage, oxidative stress, hypoxia, and infections can initiate signaling cascades leading to nuclear degradation through the intrinsic pathway of apoptosis.

[3] In necrosis, uncontrolled calcium influx and activation of proteases such as calpains accelerate the process, highlighting the contrasting regulatory mechanisms between necrotic and apoptotic karyorrhexis.

[14] Moreover, disorders such as placental vascular malperfusion have highlighted the role of karyorrhexis in fetal demise, particularly when it disrupts normal tissue homeostasis.