Association of heat shock proteins with all-cause mortality
Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell...
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2012
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pubmed-37050922013-07-11 Association of heat shock proteins with all-cause mortality Broer, L. Demerath, E. W. Garcia, M. E. Homuth, G. Kaplan, R. C. Lunetta, K. L. Tanaka, T. Tranah, G. J. Walter, S. Arnold, A. M. Atzmon, G. Harris, T. B. Hoffmann, W. Karasik, D. Kiel, D. P. Kocher, T. Launer, L. J. Lohman, K. K. Rotter, J. I. Tiemeier, H. Uitterlinden, A. G. Wallaschofski, H. Bandinelli, S. Dörr, M. Ferrucci, L. Franceschini, N. Gudnason, V. Hofman, A. Liu, Y. Murabito, J. M. Newman, A. B. Oostra, B. A. Psaty, B. M. Smith, A. V. van Duijn, C. M. Article Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell death, and recent experiments indicate a highly versatile role for these proteins as inhibitors of programmed cell death. In this study, we examined common genetic variations in 31 genes encoding all members of the HSP70, small HSP, and heat shock factor (HSF) families for their association with all-cause mortality. Our discovery cohort was the Rotterdam study (RS1) containing 5,974 participants aged 55 years and older (3,174 deaths). We assessed 4,430 single nucleotide polymorphisms (SNPs) using the HumanHap550K Genotyping BeadChip from Illumina. After adjusting for multiple testing by permutation analysis, three SNPs showed evidence for association with all-cause mortality in RS1. These findings were followed in eight independent population-based cohorts, leading to a total of 25,007 participants (8,444 deaths). In the replication phase, only HSF2 (rs1416733) remained significantly associated with all-cause mortality. Rs1416733 is a known cis-eQTL for HSF2. Our findings suggest a role of HSF2 in all-cause mortality. Springer Netherlands 2012-05-04 2013-08 /pmc/articles/PMC3705092/ /pubmed/22555621 http://dx.doi.org/10.1007/s11357-012-9417-7 Text en © The Author(s) 2012 |
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Open Access Journal |
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Foreign Institution |
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US National Center for Biotechnology Information |
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NCBI PubMed |
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Online Access |
language |
English |
format |
Online |
author |
Broer, L. Demerath, E. W. Garcia, M. E. Homuth, G. Kaplan, R. C. Lunetta, K. L. Tanaka, T. Tranah, G. J. Walter, S. Arnold, A. M. Atzmon, G. Harris, T. B. Hoffmann, W. Karasik, D. Kiel, D. P. Kocher, T. Launer, L. J. Lohman, K. K. Rotter, J. I. Tiemeier, H. Uitterlinden, A. G. Wallaschofski, H. Bandinelli, S. Dörr, M. Ferrucci, L. Franceschini, N. Gudnason, V. Hofman, A. Liu, Y. Murabito, J. M. Newman, A. B. Oostra, B. A. Psaty, B. M. Smith, A. V. van Duijn, C. M. |
spellingShingle |
Broer, L. Demerath, E. W. Garcia, M. E. Homuth, G. Kaplan, R. C. Lunetta, K. L. Tanaka, T. Tranah, G. J. Walter, S. Arnold, A. M. Atzmon, G. Harris, T. B. Hoffmann, W. Karasik, D. Kiel, D. P. Kocher, T. Launer, L. J. Lohman, K. K. Rotter, J. I. Tiemeier, H. Uitterlinden, A. G. Wallaschofski, H. Bandinelli, S. Dörr, M. Ferrucci, L. Franceschini, N. Gudnason, V. Hofman, A. Liu, Y. Murabito, J. M. Newman, A. B. Oostra, B. A. Psaty, B. M. Smith, A. V. van Duijn, C. M. Association of heat shock proteins with all-cause mortality |
author_facet |
Broer, L. Demerath, E. W. Garcia, M. E. Homuth, G. Kaplan, R. C. Lunetta, K. L. Tanaka, T. Tranah, G. J. Walter, S. Arnold, A. M. Atzmon, G. Harris, T. B. Hoffmann, W. Karasik, D. Kiel, D. P. Kocher, T. Launer, L. J. Lohman, K. K. Rotter, J. I. Tiemeier, H. Uitterlinden, A. G. Wallaschofski, H. Bandinelli, S. Dörr, M. Ferrucci, L. Franceschini, N. Gudnason, V. Hofman, A. Liu, Y. Murabito, J. M. Newman, A. B. Oostra, B. A. Psaty, B. M. Smith, A. V. van Duijn, C. M. |
author_sort |
Broer, L. |
title |
Association of heat shock proteins with all-cause mortality |
title_short |
Association of heat shock proteins with all-cause mortality |
title_full |
Association of heat shock proteins with all-cause mortality |
title_fullStr |
Association of heat shock proteins with all-cause mortality |
title_full_unstemmed |
Association of heat shock proteins with all-cause mortality |
title_sort |
association of heat shock proteins with all-cause mortality |
description |
Experimental mild heat shock is widely known as an intervention that results in extended longevity in various models along the evolutionary lineage. Heat shock proteins (HSPs) are highly upregulated immediately after a heat shock. The elevation in HSP levels was shown to inhibit stress-mediated cell death, and recent experiments indicate a highly versatile role for these proteins as inhibitors of programmed cell death. In this study, we examined common genetic variations in 31 genes encoding all members of the HSP70, small HSP, and heat shock factor (HSF) families for their association with all-cause mortality. Our discovery cohort was the Rotterdam study (RS1) containing 5,974 participants aged 55 years and older (3,174 deaths). We assessed 4,430 single nucleotide polymorphisms (SNPs) using the HumanHap550K Genotyping BeadChip from Illumina. After adjusting for multiple testing by permutation analysis, three SNPs showed evidence for association with all-cause mortality in RS1. These findings were followed in eight independent population-based cohorts, leading to a total of 25,007 participants (8,444 deaths). In the replication phase, only HSF2 (rs1416733) remained significantly associated with all-cause mortality. Rs1416733 is a known cis-eQTL for HSF2. Our findings suggest a role of HSF2 in all-cause mortality. |
publisher |
Springer Netherlands |
publishDate |
2012 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705092/ |
_version_ |
1611993003908399104 |