Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add filters








Language
Year range
1.
Iranian Journal of Basic Medical Sciences. 2008; 11 (3): 121-142
in English | IMEMR | ID: emr-103248

ABSTRACT

Apoptosis or programmed cell death is a gene regulated phenomenon which is important in both physiological and pathological conditions. It is characterized by distinct morphological features including chromatin condensation, cell and nuclear shrinkage, membrane blebbing and oligonucleosomal DNA fragmentation. Although, two major apoptotic pathways including 1] the death receptor [extrinsic] and 2] mitochondrial [intrinsic] pathway have been identified, recently endoplasmic reticulum and lysosomal pathways have been also recognized. Depending on both the cell type and the initiating factor, distinct pathways are activated. The pathways share a common final phase of apoptosis, consisting of activation of the executioner caspases and dismantling of substrates critical for cell survival. The important regulatory mechanisms include death receptors, caspases, mitochondria and Bcl-2 family proteins. Modulating of apoptosis is a novel therapeutic strategy in treatment of different diseases. These include situations with unwanted cell accumulation [cancer] and failure to diminish aberrant cells [autoimmune diseases] or diseases with an inappropriate cell loss [heart failure, stroke, AIDS and neurodegenerative diseases]. Modulation of apoptosis is a novel therapeutic strategy in treatment of different diseases. Many approaches including gene therapy, antisense strategies and numerous apoptotic drugs to target specific apoptotic regulators, are currently being developed. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, signaling as well as a discussion of apoptosis in diseases and effective therapy


Subject(s)
Receptors, Death Domain , Neurodegenerative Diseases , Autoimmunity , Necrosis , Neoplasms
SELECTION OF CITATIONS
SEARCH DETAIL