As mentioned before

As mentioned before, ion homeostasis is linked to apoptosis and bioelectrical properties can be used as indicators for cell characterization and can control cell development, therefore the plasma membrane potential is apt to be linked to apoptosis.
Many studies reported a plasma membrane depolarization accompanied cell apoptosis (2001, Bortner; 2006, Franco). But the role of this depolarization during cell death is still not clear. PMP depolarization through apoptosis may be a consequence of ionic imbalance or it may be a signal required is initiating the required factors of apoptotic.
Since cell apoptotic is reported to be initiated with an imbalance in major ions such as K+, Na+, Ca2+ and Cl- (2004, Nolte; ((1995) Barbiero, (1995) Beauvais, 1997, Bortner, 1998, Dallaporta, 1997, Hughes, (2000) Nobel, 2000, Yu; 2012, Lobikin), and these ions are known to be correlated with the generation of the resting membrane potential (see section PMP), PMP may be a consequence of the imbalance in these ions. A huge decrease in intracellular K+ concentration was reported the development of cell apoptosis. In addition, an increase of Na+ and Ca2+ intracellular concentrations were observed in the apoptotic process (2001, Bortner, 2004, Nolte). These results may support that the PMP is a consequence of ionic imbalance during apoptosis. But, lowering extracellular Cl- which results in membrane depolarization and apoptosis may correlate apoptosis to the depolarization of the membrane. Since changes in extracellular Cl- without a change in osmotic pressure will not result in cell shrinkage and AVD, whereas the influx of Na+ and Ca2+ which result in cell swelling and membrane depolarization. The depolarization of the membrane causes the efflux of K+, which result in an osmotic imbalance and shrinkage of the cell volume.
From all these studies it is not obvious if the depolarization is a required factor in apoptosis even it precedes K+ efflux and shrinkage because shrinkage and apoptosis may be initiated by a dysfunction of regulatory volume increase which may result in shrinkage due to upregulation of aquaporins (APQs see reviews by (1999) Borgnia, (2003) Brown, (1998) BROWN, (2000) King)) then inactivation of these water pathways. But, the depolarization of the PM may be required in cases where apoptosis is initiated by the huge loss of K+ due to depolarization which results in shrinkage and cytochrome c release.