Related Experiment Video
Updated: May 29, 2025

Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
Published on: April 1, 2011
CaMKII at the crossroads: calcium dysregulation, and post-translational modifications driving cell death
Alicia Mattiazzi1, Carolina Jaquenod De Giusti1, Carlos A Valverde1
1Centro de Investigaciones Cardiovasculares 'Dr Horacio E. Cingolani,' CCT-La Plata/CONICET, Facultad de Ciencias Médicas, UNLP, La Plata, Argentina.
None:
The multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) regulates numerous proteins involved in excitation-contraction-relaxation coupling and cardiac excitability. However, its overactivation induces severe Ca2+/handling alterations, playing a significant role in the pathogenesis of diseases such as hypertrophy, arrhythmias and cell death, which can ultimately lead to heart failure. Being a suitable target for various aberrant signals that characterize several diseases, such as Ca2+ overload, oxidative stress or excessive glycosylation, CaMKII shifts under these conditions from a physiological regulator to a pathological molecule. In this review, we explore the evolution of knowledge regarding the role of CaMKII activation on cell death across different pathological contexts, focusing on the converging mechanisms that transform the enzyme from an ally into a villain.
Related Concept Videos
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
MAPK Signaling Cascades
Caspases
Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Regulation of the Unfolded Protein Response
cAMP-dependent Protein Kinase Pathways

