Apoptosis: A Review of Programmed Cell Death

Abstract

The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.

Heterogeneity of fatty acid metabolism in breast cancer cells underlies differential sensitivity to palmitate‐induced apoptosis

“…This reduced reductive metabolic capacity (measured via MTT assay) was associated with activation of PARP and ATF4 signaling after 1 day of palmitate treatment (Fig. 3C), which are markers of apoptosis (Elmore, 2007; Sano and Reed, 2013). Further, the early activation of apoptotic signaling corresponded with reduced cell number (Fig.…”

Soluble CD74 Reroutes MIF/CXCR4/AKT‐Mediated Survival of Cardiac Myofibroblasts to Necroptosis

“…In order to identify mechanisms underlying the synergistic cell‐death–promoting effect of sCD74/MIF co‐treatment in myofibroblasts, we analyzed cleaved caspase‐3 levels as an indication of apoptosis execution51 using Western blot methodology. We observed no significant changes of cleaved caspase‐3 at 10 hours after stimulation (Figure 2A and 2B), which has been previously shown to be an appropriate time window for late caspase activation 52.…”

Amyloid‐beta 1‐40 is associated with alterations in NG2+ pericyte population ex vivo and in vitro

“…We therefore analysed activity of caspases 3 and 7 (the two most prominent executor caspases in the apoptosis pathway (Elmore, 2007)) in HBVP after exposure to the three different aggregation forms of Aβ1‐40 and Aβ1‐42. Our analysis showed significantly increased caspase 3/7 activity after 24‐hr exposure to fibril‐EP Aβ1‐40 compared to Ctrl O/F (67032.83 ± 3342.54 vs. 58101.83 ± 3395.34, p  =   .021; Figure 4a), but unaltered caspase 3/7 activity after 24‐hr exposure of oligomer‐EP Aβ1‐40 compared to Ctrl O/F (52530.17 ± 2988.63 vs. 58101.83 ± 3395.34, p  =   .170; Figure 4a).…”