The Role of Apoptosis in Sepsis-Induced Kidney Dysfunction


  • Jo A. Crum Elon University
  • Victoria Del Gaizo Moore Elon University



Sepsis, Apotposis, BCL2, Acute Kidney Injury, Inflammation, Immunity


Sepsis is a system-wide inflammatory response to infection in the blood, which can be caused by any type of pathogen such as bacteria or fungi. During severe sepsis, end-organs often shut down as the body goes into shock, causing irreparable damage and eventual fatality. Even though sepsis is the third highest cause of death in the world, only one third of Americans have heard of the condition. Such unawareness reflects the deficit in knowledge about of how end-organ damage that results from sepsis. Consequently, most current treatments for sepsis address symptoms rather than the cause. While the effects of sepsis on immune cells have been thoroughly examined, the effect on other organs, such as the kidneys, has not been elucidated. In septic patients, a condition caused by excessive cell death resulting in massive tissue damage called acute kidney injury (AKI), becomes considerably more dangerous in septic patients, doubling the mortality rate of AKI. Programmed cell death, otherwise known as apoptosis, is a natural form of cell death, and is only damaging when it behaves in an irregular manner such as not being triggered in cancer cells or excessively occurring after ischemia-reperfusion. Apoptosis is one mechanism that is thought to be responsible for AKI during sepsis, and therefore studying apoptotic  regulatory proteins  may provide insight into how renal cell death occurs during sepsis-induced AKI (SI-AKI).  Furthermore, unraveling the molecular mechanism of kidney cell death could lead to the development of more effective treatments or preventative measures for this widespread condition.


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Author Biography

Jo A. Crum, Elon University

Chemistry Department, Elon University

Elon College Fellow



How to Cite

Crum, J. A., & Del Gaizo Moore, V. (2012). The Role of Apoptosis in Sepsis-Induced Kidney Dysfunction. Journal of Student Research, 1(3), 1-8.



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