Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury
Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury. Though much is known regarding the gross pathology of SM injury, the molecular and cellular basis for this pathology is not well understood. General cellular processes such as inflammation, DNA damag...
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| Format: | Online |
| Language: | English |
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Open Science Company, LLC
2007
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2206000/ |
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pubmed-22060002008-01-22 Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury Ruff, Albert L. Dillman, James F. Article Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury. Though much is known regarding the gross pathology of SM injury, the molecular and cellular basis for this pathology is not well understood. General cellular processes such as inflammation, DNA damage response, and apoptosis have been hypothesized to be involved in SM injury. However, the specific molecules, signaling pathways, and gene products involved in the pathogenesis of SM injury have not been elucidated. This review discusses the molecular mechanisms observed in in vivo and in vitro models of cutaneous SM injury. Methods: The historical literature on the clinical pathology of SM-induced cutaneous injury is summarized, and recent work elucidating molecular signaling pathways involved in SM toxicity is extensively reviewed. In addition, this review focuses the discussion of SM-induced molecular mechanisms on those that have been experimentally validated in models of SM injury. Results: Recent work has uncovered potential roles for a number of signaling molecules. In particular, molecules in inflammatory signaling, DNA damage response, apoptosis signaling, and calcium signaling have been implicated in SM injury. These include signaling molecules involved in inflammation (e.g. p38 MAP kinase), apoptosis (e.g. p53, NF-κ B, caspases, Fas), and cell stress responses (e.g. calcium, calmodulin). Conclusions: Many of the molecules and mechanisms implicated in SM injury are now being experimentally validated. Critical questions are proposed that remain to be answered to increase our understanding of SM toxicity and accelerate the development of vesicant therapeutics. Open Science Company, LLC 2007-11-27 /pmc/articles/PMC2206000/ /pubmed/18213398 Text en Copyright © 2007 The Author(s) http://creativecommons.org/licenses/by/2.0/ This is an open-access article whereby the authors retain copyright of the work. The article is distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Ruff, Albert L. Dillman, James F. |
| spellingShingle |
Ruff, Albert L. Dillman, James F. Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| author_facet |
Ruff, Albert L. Dillman, James F. |
| author_sort |
Ruff, Albert L. |
| title |
Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| title_short |
Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| title_full |
Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| title_fullStr |
Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| title_full_unstemmed |
Signaling Molecules in Sulfur Mustard-Induced Cutaneous Injury |
| title_sort |
signaling molecules in sulfur mustard-induced cutaneous injury |
| description |
Objective: Sulfur mustard (SM) is a potent alkylating agent that can induce severe cutaneous injury. Though much is known regarding the gross pathology of SM injury, the molecular and cellular basis for this pathology is not well understood. General cellular processes such as inflammation, DNA damage response, and apoptosis have been hypothesized to be involved in SM injury. However, the specific molecules, signaling pathways, and gene products involved in the pathogenesis of SM injury have not been elucidated. This review discusses the molecular mechanisms observed in in vivo and in vitro models of cutaneous SM injury. Methods: The historical literature on the clinical pathology of SM-induced cutaneous injury is summarized, and recent work elucidating molecular signaling pathways involved in SM toxicity is extensively reviewed. In addition, this review focuses the discussion of SM-induced molecular mechanisms on those that have been experimentally validated in models of SM injury. Results: Recent work has uncovered potential roles for a number of signaling molecules. In particular, molecules in inflammatory signaling, DNA damage response, apoptosis signaling, and calcium signaling have been implicated in SM injury. These include signaling molecules involved in inflammation (e.g. p38 MAP kinase), apoptosis (e.g. p53, NF-κ B, caspases, Fas), and cell stress responses (e.g. calcium, calmodulin). Conclusions: Many of the molecules and mechanisms implicated in SM injury are now being experimentally validated. Critical questions are proposed that remain to be answered to increase our understanding of SM toxicity and accelerate the development of vesicant therapeutics. |
| publisher |
Open Science Company, LLC |
| publishDate |
2007 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2206000/ |
| _version_ |
1611433525322448896 |