[Apoptosis or programmed cell death: regulatory and pathophysiological mechanisms (editorial)]

Important note: Information in this article was accurate in 1995. The state of the art may have changed since the publication date.

[Apoptosis or programmed cell death: regulatory and pathophysiological mechanisms (editorial)]

Ann Ital Med Int. 1995 Jan-Mar;10(1):7-13. Unique Identifier : AIDSLINE MED/95244238
Silvestris F; Ribatti D; Nico B; Silvestris N; Romito A; Dammacco F

Abstract: Apoptosis is an active death process genetically encoded to eliminate abnormal or unwanted cells. The phenomenon is induced by a cascade of molecular events leading to nucleolysis by endonucleases and involves a number of membrane receptors and cytoplasmic proteins. These structures (including Fas, mullerian inhibiting substance, p53 and the c-myc oncogene) contribute, by interactive regulatory mechanisms, to the promotion or inhibition of apoptosis, on the basis of both external stimulus and cell activation state. Since apoptosis is a selective process to suppress defective cells, deregulation of genes encoding for such apoptosis-related proteins could be relevant in the growth of several tumors. Remarkably, overexpression of the bcl-2 gene in a few experimental lymphomas has been associated with neoplastic proliferation because of its inhibitory effect on apoptosis. Conversely, early activation of Fas, an apoptosis-inducing gene on HIV-infected CD4+ lymphocytes, is thought to aggravate T cell lymphopenia in HIV infection by increasing the level of normal apoptosis. Genetic deregulation of apoptosis has also been postulated in the pathogenesis of several diseases. Indeed, while preliminary studies suggest that apoptosis plays a role in autoimmune disorders including systemic lupus erythematosus, the pathogenesis of a few degenerative neuropathies, such as Alzheimer's disease, could depend on a similar altered mechanism in apoptosis of neuronal cells. However, no studies are presently available to suggest that exploitation of molecular events of apoptosis would imply therapeutic progress.

Keywords: Acquired Immunodeficiency Syndrome/GENETICS/PATHOLOGY Alzheimer's Disease/GENETICS/PATHOLOGY Apoptosis/*GENETICS/*PHYSIOLOGY Autoimmune Diseases/GENETICS/PATHOLOGY Comparative Study Dexamethasone/PHARMACOLOGY Endonucleases/METABOLISM English Abstract Enzyme Activation Genes, myc Genes, pX Human Neoplasms/GENETICS/PATHOLOGY T-Lymphocytes/DRUG EFFECTS/PHYSIOLOGY EDITORIAL REVIEW REVIEW, TUTORIAL JOURNAL ARTICLE
950830
M9580990

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