MICU1 may be a promising intervention target for gut-derived sepsis induced by intra-abdominal hypertension

Leng, Yuxin; Ge, Qi; Zhao, Zhiling; Wang, Kun; Yao, Gaiqi

doi:10.1038/cddiscovery.2016.80

Cited by 5 publications

(3 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been demonstrated that FOXD1-dependent MICU1 expression regulates mitochondrial activity and cell differentiation [ 25 ]. Leng et al [ 26 ] revealed that MICU-related oxidation/antioxidation disequilibrium is strongly involved in intra-abdominal hypertension-induced damage to intestinal barriers. Another study revealed that MICU1 deficiency is associated with mitochondrial Ca 2+ uptake during aerobic metabolism impairment, muscle weakness and myofiber damage during physical activity [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway

Yang¹,

Du²,

Xu³

et al. 2020

Aging

View full text Add to dashboard Cite

Mitochondrial calcium uptake 1 (MICU1) is a pivotal molecule in maintaining mitochondrial homeostasis under stress conditions. However, it is unclear whether MICU1 attenuates mitochondrial stress in angiotensin II (Ang-II)-induced cardiac hypertrophy or if it has a role in the function of melatonin. Here, small-interfering RNAs against MICU1 or adenovirus-based plasmids encoding MICU1 were delivered into left ventricles of mice or incubated with neonatal murine ventricular myocytes (NMVMs) for 48 h. MICU1 expression was depressed in hypertrophic myocardia and MICU1 knockdown aggravated Ang-II-induced cardiac hypertrophy in vivo and in vitro . In contrast, MICU1 upregulation decreased cardiomyocyte susceptibility to hypertrophic stress. Ang-II administration, particularly in NMVMs with MICU1 knockdown, led to significantly increased reactive oxygen species (ROS) overload, altered mitochondrial morphology, and suppressed mitochondrial function, all of which were reversed by MICU1 supplementation. Moreover, peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α)/MICU1 expression in hypertrophic myocardia increased with melatonin. Melatonin ameliorated excessive ROS generation, promoted mitochondrial function, and attenuated cardiac hypertrophy in control but not MICU1 knockdown NMVMs or mice. Collectively, our results demonstrate that MICU1 attenuates Ang-II-induced cardiac hypertrophy by inhibiting mitochondria-derived oxidative stress. MICU1 activation may be the mechanism underlying melatonin-induced protection against myocardial hypertrophy.

show abstract

Section: Discussionmentioning

confidence: 99%

Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway

Yang¹,

Du²,

Xu³

et al. 2020

Aging

View full text Add to dashboard Cite

show abstract

“…Rats fasted for 12 h while water was free to access before operation. The IAH model was established according to the method previously described (Gong et al, 2011;Leng et al, 2016). In brief, rats were anesthetized with sodium pentobarbital 40 mg/kg by intraperitoneal injection.…”

Section: Intra-abdominal Hypertension Model Establishedmentioning

confidence: 99%

Gut Microbiota Was Involved in the Process of Liver Injury During Intra-Abdominal Hypertension

et al. 2021

View full text Add to dashboard Cite

Background: Intestinal damage caused by intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) can lead to the ectopic gut microbiota, which can contribute to liver injury via portal veins. Therefore, it is speculated that gut microbiota disorder caused by IAH/ACS may result in liver injury. The relationship between gut microbiota and IAH/ACS-related liver injury was investigated in this study.Methods: A model of IAH was established in rats, and 16S rRNA sequencing was analyzed for gut microbiota in the feces of rats. The elimination of gut microbiota was completed by antibiotics gavage, and fecal microbiota transplantation (FMT) was used to change the composition of gut microbiota in rats.Results: In addition to the traditional cause of liver blood vessel compression, liver injury caused by IAH was also associated with gut microbiota dysbiosis. Gut microbiota clearance can relieve liver injury caused by IAH, while FMT from IAH-intervened rats can aggravate IAH-related liver injury.Conclusion: The gut microbiota was one of the most important factors contributing to the IAH-related liver injury, and the JNK/p38 signaling pathway was activated in this process.

show abstract

“…In a recent experimental study, Leng et al [37] indicated that mitochondrial Ca 2+ uptake 1 (MICU1)-related oxidation/antioxidation disequilibrium is strongly involved in IAH-induced damage to intestinal barriers. MICU1-targeted treatment may hold promise for preventing the progression of IAH to gut-derived sepsis.…”

Section: Recent Insightsmentioning

confidence: 99%

Abdominal Compartment Syndrome: What Is New?

Tharayil¹,

Ganaw²,

Abdulrahman³

et al. 2017

Intensive Care

View full text Add to dashboard Cite

Intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are continuation of the same pathological and physiological processes that are largely unrecognized in critical patients. From an era of indistinct definitions and recommendations, this condition has been studied extensively and experts have come forward with clear definitions and recommendations for management. IAH is graded in four grades and ACS is IAH above 20 cm H 2 O with new organ dysfunction. IAH/ACS can present as acute, hyperacute, or chronic and aetiologically can be classified into primary, secondary and tertiary. It affects various body systems including respiratory, cardiovascular, central nervous, gastrointestinal, renal and hepatic systems adversely and results in deleterious consequences. Management of IAH/ACS is based on the evacuation of intra-luminal and extra-luminal contents, improving the abdominal wall compliance. There are various surgical techniques recommended for preventing the development of IAH/ACS and mitigating the negative consequences. New medical therapies such as octreotide, tissue plasminogen activator, melatonin and vitamin C are being investigated and non-pharmacological methods such as continuous negative abdominal pressure (CNAP) have been introduced recently but are still experimental and not recommended for routine use.

show abstract

MICU1 may be a promising intervention target for gut-derived sepsis induced by intra-abdominal hypertension

Cited by 5 publications

References 28 publications

Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway

Melatonin alleviates angiotensin-II-induced cardiac hypertrophy via activating MICU1 pathway

Gut Microbiota Was Involved in the Process of Liver Injury During Intra-Abdominal Hypertension

Abdominal Compartment Syndrome: What Is New?

Contact Info

Product

Resources

About