pubmed-article:16799139 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16799139 | lifeskim:mentions | umls-concept:C0008679 | lld:lifeskim |
pubmed-article:16799139 | lifeskim:mentions | umls-concept:C0001811 | lld:lifeskim |
pubmed-article:16799139 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
pubmed-article:16799139 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:16799139 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:16799139 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:16799139 | pubmed:dateCreated | 2006-6-26 | lld:pubmed |
pubmed-article:16799139 | pubmed:abstractText | The human interleukin IL-6 was originally cloned in 1986. In 1993, William Ershler, in his article "IL-6: A Cytokine for Gerontologists," indicated IL-6 as one of the main signaling pathways modulating the complex relationship between aging and chronic morbidity. Over the last 12 years, our understanding of the role of IL-6 in human physiology and pathology has substantially grown, although some of the questions originally posed by Ershler are still debated. In this review, we will focus on IL-6 structure, IL-6 signaling, and trans signaling pathways, and the role of IL-6 in geriatric syndromes and chronic disease. In the final section of this review, we dissect the critical elements of the IL-6 signaling pathway and point out targets for intervention that are targeted by emerging drugs, some still on the horizon and others already being tested in clinical trials. | lld:pubmed |
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