Apoptosis in the Pathogenesis and Treatment of Disease
Abstract
In multicellular organisms, homeostasis is maintained through a balance between cell proliferation and cell death. Although much is known about the control of cell proliferation, less is known about the control of cell death. Physiologic cell death occurs primarily through an evolutionarily conserved form of cell suicide termed apoptosis. The decision of a cell to undergo apoptosis can be influenced by a wide variety of regulatory stimuli. Recent evidence suggests that alterations in cell survival contribute to the pathogenesis of a number of human diseases, including cancer, viral infections, autoimmune diseases, neurodegenerative disorders, and AIDS (acquired immunodeficiency syndrome). Treatments designed to specifically alter the apoptotic threshold may have the potential to change the natural progression of some of these diseases.
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Cells dying by apoptosis can be vigorously immunogenic, whereas necrotic cells can be less immunogenic than cells undergoing an immunogenic form of apoptosis.
“However, in-depth investigations have shown that cells dying by apoptosis can be vigorously immunogenic, whereas necrotic cells can be less immunogenic than cells undergoing an immunogenic form of apoptosis 2,6.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [6]
A chemical caspase inhibitor or transfection with a caspase inhibitor destroyed the capacity of anthracyclin-treated cancer cells to induce anti-tumour immune responses after subcutaneous administration.
“A chemical caspase inhibitor (zVAD-fmk) or transfection with a caspase inhibitor (such as baculovirus p35) destroyed the capacity of anthracyclin-treated cancer cells to induce anti-tumour immune responses following their subcutaneous administration6.”
From Immunogenic and tolerogenic cell death (2009) · cites this paper as [6]
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Aging alters the reduction of pro-apoptotic signaling in response to loading-induced hypertrophy
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- Authors
- Thompson, C. B.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Thompson, Craig B.
- ORCID
- Thompson, Craig B.
- Venue
- Science
- Published
- 1995-03-10
- Volume
- 267
- Issue
- 5203
- Pages
- 1456-1462
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W1991865867
- Cited by
- 6,524
- References
- 145
- Citations by year
- 2026: 19 · 2025: 35 · 2024: 43 · 2023: 58 · 2022: 49 · 2021: 75 · 2020: 86 · 2019: 76 · 2018: 100 · 2017: 114 · 2016: 119 · 2015: 149 · 2014: 131 · 2013: 193 · 2012: 184
- FWCI
- 33.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- apoptosis, cell death regulation, cell proliferation, homeostasis, cancer, viral infection, autoimmune disease, neurodegenerative diseases, AIDS, apoptosis inhibitor, pathogenesis
- MeSH terms
- Acquired Immunodeficiency Syndrome, Animals, Autoimmune Diseases, Cell Division, Cell Survival, Disease, Hematologic Diseases, Humans, Neoplasms, Nervous System Diseases, Therapeutics, Virus Diseases, Apoptosis
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