Alternate Day Calorie Restriction Improves Systemic Inflammation in a Mouse Model of Sepsis Induced by Cecal Ligation and Puncture

Hasegawa, Akira; Iwasaka, Hideo; Hagiwara, Satoshi; Asai, Nobuhiko; Nishida, Taichi; Noguchi, Takayuki

doi:10.1016/j.jss.2010.11.883

Cited by 24 publications

(13 citation statements)

References 22 publications

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“…It is important to note that the nucleus-to-cytoplasm translocation of HMGB1 is not an active process. Previous studies have confirmed that the functions of HMGB1 depend on its molecular localization and posttranslational modifications (8,18,21). Of note, SIRT1-mediated deacetylation of HMGB1 has received substantial attention during past decades.…”

Section: Discussionmentioning

confidence: 87%

“…Of note, SIRT1-mediated deacetylation of HMGB1 has received substantial attention during past decades. SIRT1 activation via calorie restriction is reported to attenuate sepsisinduced inflammation in a CLP-induced mouse model (8). In one study, male C57BL/6N mice underwent alternate day calorie restriction for 8 days before CLP-induced sepsis, and it was found that the serum cytokine and HMGB1 levels were lower in the animals that underwent calorie restriction compared with normally fed mice after CLP treatment (8).…”

Section: Discussionmentioning

confidence: 99%

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SIRT1-mediated HMGB1 deacetylation suppresses sepsis-associated acute kidney injury

Wei

Gao

Dai

et al. 2019

American Journal of Physiology-Renal Physiology

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Sepsis is the leading cause of death in the intensive care unit and continues to lack effective treatment. It is widely accepted that high-mobility group box 1 (HMGB1) is a key inflammatory mediator in the pathogenesis of sepsis. Moreover, some studies indicate that the functions of HMGB1 depend on its molecular localization and posttranslational modifications. Our previous study confirms that sirtuin 1, silent information regulator 2-related enzyme 1 (SIRT1), a type III deacetylase, can ameliorate sepsis-associated acute kidney injury (SA-AKI). We explored the effect and mechanism of SIRT1 on HMGB1 using a mouse model of cecal ligation and puncture-induced sepsis and LPS-treated human kidney (HK-2) cell line. We found that HMGB1 is elevated in the serum but is gradually reduced in kidney cells in the later stages of septic mice. The acetylation modification of HMGB1 is a key process before its nucleus-to-cytoplasm translocation and extracellular secretion in kidney cells, accelerating the development of SA-AKI. Moreover, SIRT1 can physically interact with HMGB1 at the deacetylated lysine sites K28, K29, and K30, subsequently suppressing downstream inflammatory signaling. Thus the SIRT1-HMGB1 signaling pathway is a crucial mechanism in the development of SA-AKI and presents a novel experimental perspective for future SA-AKI research.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

SIRT1-mediated HMGB1 deacetylation suppresses sepsis-associated acute kidney injury

Wei

Gao

Dai

et al. 2019

American Journal of Physiology-Renal Physiology

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“…Outcomes appear to depend on the CR regimen as well as the infectious agent. For example, Hasegawa et al (2012) subjected male B6 mice to 8 days of EOD before CLG cecal ligation(Hasegawa et al, 2012). They noted decreased mortality in CR mice, less organ injury, and reduced inflammatory response.…”

Section: Are There Detrimental Effects Of Cr?mentioning

confidence: 99%

Calorie restriction in rodents: Caveats to consider

Ingram

Cabo

2017

Ageing Research Reviews

108

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The calorie restriction paradigm has provided one of the most widely used and most useful tools for investigating mechanisms of aging and longevity. By far, rodent models have been employed most often in these endeavors. Over decades of investigation, claims have been made that the paradigm produces the most robust demonstration that aging is malleable. In the current review of the rodent literature, we present arguments that question the robustness of the paradigm to increase lifespan and healthspan. Specifically, there are several questions to consider as follows: (1) At what age does CR no longer produce benefits? (2) Does CR attenuate cognitive decline? (3) Are there negative effects of CR, including effects on bone health, wound healing, and response to infection? (4) How important is schedule of feeding? (5) How long does CR need to be imposed to be effective? (6) How do genotype and gender influence CR? (7) What role does dietary composition play? Consideration of these questions produce many caveats that should guide future investigations to move the field forward.

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“…Additionally, CR can improve insulin sensitivity through regulating the insulin-and IGF-1-signaling and autophagy pathways [119, 120]. CR or fasting improves systemic inflammation in sepsis and ischemic injury partly through reduction of the release of DAMPs such as HMGB1 [121, 122]. In addition, the reduction in serum HMGB1 appears to be mediated by the NAD-dependent protein deacetylase sirtuin-1-associated autophagic response [122].…”

Section: The Common Hallmarks Of Ageing and Cancermentioning

confidence: 99%

DAMPs, ageing, and cancer: The ‘DAMP Hypothesis’

Huang

Xie

Sun

et al. 2015

Ageing Research Reviews

122

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Ageing is a complex and multifactorial process characterized by the accumulation of many forms of damage at the molecular, cellular, and tissue level with advancing age. Ageing increases the risk of the onset of chronic inflammation-associated diseases such as cancer, diabetes, stroke, and neurodegenerative disease. In particular, ageing and cancer share some common origins and hallmarks such as genomic instability, epigenetic alteration, aberrant telomeres, inflammation and immune injury, reprogrammed metabolism, and degradation system impairment (including within the ubiquitin-proteasome system and the autophagic machinery). Recent advances indicate that damage-associated molecular pattern molecules (DAMPs) such as high mobility group box 1, histones, S100, and heat shock proteins play location-dependent roles inside and outside the cell. These provide interaction platforms at molecular levels linked to common hallmarks of ageing and cancer. They can act as inducers, sensors, and mediators of stress through individual plasma membrane receptors, intracellular recognition receptors (e.g., advanced glycosylation end product-specific receptors, AIM2-like receptors, RIG-I-like receptors, and NOD1-like receptors, and toll-like receptors), or following endocytic uptake. Thus, the DAMP Hypothesis is novel and complements other theories that explain the features of ageing. DAMPs represent ideal biomarkers of ageing and provide an attractive target for interventions in ageing and age-associated diseases.

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Alternate Day Calorie Restriction Improves Systemic Inflammation in a Mouse Model of Sepsis Induced by Cecal Ligation and Puncture

Cited by 24 publications

References 22 publications

SIRT1-mediated HMGB1 deacetylation suppresses sepsis-associated acute kidney injury

SIRT1-mediated HMGB1 deacetylation suppresses sepsis-associated acute kidney injury

Calorie restriction in rodents: Caveats to consider

DAMPs, ageing, and cancer: The ‘DAMP Hypothesis’

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