Experimental sepsis‐induced mitochondrial biogenesis is dependent on autophagy, TLR4, and TLR9 signaling in liver-Reference-Cited by-同舟云学术

Experimental sepsis‐induced mitochondrial biogenesis is dependent on autophagy, TLR4, and TLR9 signaling in liver

Published:2013-08-27 Issue:12 Volume:27 Page:4703-4711
ISSN:0892-6638
Container-title:The FASEB Journal
language:en
Short-container-title:FASEB j.

Author:

Carchman Evie H.¹²,Whelan Sean¹,Loughran Patricia¹²,Mollen Kevin¹,Stratamirovic Sladjana¹²,Shiva Sruti³⁴,Rosengart Matthew R.¹,Zuckerbraun Brian S.¹⁴²

Affiliation:

1. Department of SurgeryUniversity of PittsburghPittsburghPennsylvaniaUSA

2. Veterans Affairs Pittsburgh Healthcare SystemPittsburghPennsylvaniaUSA

3. Department of PharmacologyUniversity of PittsburghPittsburghPennsylvaniaUSA

4. Vascular Medicine InstituteUniversity of PittsburghPittsburghPennsylvaniaUSA

Funder

National Institutes of Health

U.S. Department of Veterans Affairs

U.S. Department of Defense

Publisher

Wiley

Subject

Genetics,Molecular Biology,Biochemistry,Biotechnology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1096/fj.13-229476

Reference36 articles.

1. Mitochondrial dysfunction in a long-term rodent model of sepsis and organ failure

2. Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation

3. Carbon monoxide signalsviainhibition of cytochromecoxidase and generation of mitochondrial reactive oxygen species

4. Autophagy fights disease through cellular self-digestion

5. Heme oxygenase-1-mediated autophagy protects against hepatocyte cell death and hepatic injury from infection/sepsis in mice

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