Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways.
Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways.
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DOI:
10.1371/journal.pone.0062817
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Libermann TA
中科院分区:
文献类型:
--
作者:
Bhasin MK;Dusek JA;Chang BH;Joseph MG;Denninger JW;Fricchione GL;Benson H;Libermann TA
The relaxation response (RR) is the counterpart of the stress response. Millennia-old practices evoking the RR include meditation, yoga and repetitive prayer. Although RR elicitation is an effective therapeutic intervention that counteracts the adverse clinical effects of stress in disorders including hypertension, anxiety, insomnia and aging, the underlying molecular mechanisms that explain these clinical benefits remain undetermined. To assess rapid time-dependent (temporal) genomic changes during one session of RR practice among healthy practitioners with years of RR practice and also in novices before and after 8 weeks of RR training, we measured the transcriptome in peripheral blood prior to, immediately after, and 15 minutes after listening to an RR-eliciting or a health education CD. Both short-term and long-term practitioners evoked significant temporal gene expression changes with greater significance in the latter as compared to novices. RR practice enhanced expression of genes associated with energy metabolism, mitochondrial function, insulin secretion and telomere maintenance, and reduced expression of genes linked to inflammatory response and stress-related pathways. Interactive network analyses of RR-affected pathways identified mitochondrial ATP synthase and insulin (INS) as top upregulated critical molecules (focus hubs) and NF-κB pathway genes as top downregulated focus hubs. Our results for the first time indicate that RR elicitation, particularly after long-term practice, may evoke its downstream health benefits by improving mitochondrial energy production and utilization and thus promoting mitochondrial resiliency through upregulation of ATPase and insulin function. Mitochondrial resiliency might also be promoted by RR-induced downregulation of NF-κB-associated upstream and downstream targets that mitigates stress.
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影响因子:
10.6
作者:
Antoni, Michael H.;Lutgendorf, Susan K.;Blomberg, Bonnie;Carver, Charles S.;Lechner, Suzanne;Diaz, Alain;Stagl, Jamie;Arevalo, Jesusa M. G.;Cole, Steven W.
通讯作者:
Cole, Steven W.
影响因子:
5.2
作者:
Epel E;Daubenmier J;Moskowitz JT;Folkman S;Blackburn E
通讯作者:
Blackburn E
DOI:
10.1002/art.10416
发表时间:
2002-06-15
期刊:
ARTHRITIS & RHEUMATISM-ARTHRITIS CARE & RESEARCH
影响因子:
--
作者:
Astin, JA;Beckner, W;Berman, B
通讯作者:
Berman, B
影响因子:
--
作者:
Fisher, RA
通讯作者:
Fisher, RA
DOI:
10.1164/rccm.200406-710st
发表时间:
2005-04-15
影响因子:
24.7
作者:
American Thoracic Society;European Respiratory Society
通讯作者:
European Respiratory Society