About: Angiotensin-converting enzyme 2 regulates endoplasmic reticulum stress and mitochondrial function to preserve skeletal muscle lipid metabolism

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About: Angiotensin-converting enzyme 2 regulates endoplasmic reticulum stress and mitochondrial function to preserve skeletal muscle lipid metabolism Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Angiotensin-converting enzyme 2 regulates endoplasmic reticulum stress and mitochondrial function to preserve skeletal muscle lipid metabolism
Creator	Cao, Xi Yang, Jin-Kui Xin, Zhong Cheng, Zhi-Qiang Liu, Jing-Yi Lu, Xin-Meng Song, Li-Ni Tuo, Xiu Zhang, Yi-Chen
Source	PMC
abstract	OBJECTIVE: Endoplasmic reticulum (ER) stress and mitochondrial function affected intramuscular fat accumulation. However, there is no clear evident on the effect of the regulation of ER stress and mitochondrial function by Angiotensin-converting enzyme 2 (ACE2) on the prevention of intramuscular fat metabolism. We investigated the effects of ACE2 on ER stress and mitochondrial function in skeletal muscle lipid metabolism. METHODS: The triglyceride (TG) content in skeletal muscle of ACE2 knockout mice and Ad-ACE2-treated db/db mice were detected by assay kits. Meanwhile, the expression of lipogenic genes (ACCα, SREBP-1c, LXRα, CPT-1α, PGC-1α and PPARα), ER stress and mitochondrial function related genes (GRP78, eIF2α, ATF4, BCL-2, and SDH6) were analyzed by RT-PCR. Lipid metabolism, ER stress and mitochondrial function related genes were analyzed by RT-PCR in ACE2-overexpression C2C12 cell. Moreover, the IKKβ/NFκB/IRS-1 pathway was determined using lysate sample from skeletal muscle of ACE2 knockout mice. RESULTS: ACE2 deficiency in vivo is associated with increased lipid accumulation in skeletal muscle. The ACE2 knockout mice displayed an elevated level of ER stress and mitochondrial dysfunctions in skeletal muscle. In contrast, activation of ACE2 can ameliorate ER stress and mitochondrial function, which slightly accompanied by reduced TG content and down-regulated the expression of skeletal muscle lipogenic proteins in the db/db mice. Additionally, ACE2 improved skeletal muscle lipid metabolism and ER stress genes in the C2C12 cells. Mechanistically, endogenous ACE2 improved lipid metabolism through the IKKβ/NFκB/IRS-1 pathway in skeletal muscle. CONCLUSIONS: ACE2 was first reported to play a notable role on intramuscular fat regulation by improving endoplasmic reticulum and mitochondrial function. This study may provide a strategy for treating insulin resistance in skeletal muscle.
has issue date	2019-11-27(xsd:dateTime)
bibo:doi	10.1186/s12944-019-1145-x
bibo:pmid	31775868
has license	cc-by
sha1sum (hex)	f638f6e2c3362136ed83e0bfe30acaf78e7c9fb3
schema:url	https://doi.org/10.1186/s12944-019-1145-x
resource representing a document's title	Angiotensin-converting enzyme 2 regulates endoplasmic reticulum stress and mitochondrial function to preserve skeletal muscle lipid metabolism
has PubMed Central identifier	PMC6882339
has PubMed identifier	31775868
schema:publication	Lipids Health Dis
resource representing a document's body	covid:f638f6e2c3362136ed83e0bfe30acaf78e7c9fb3#body_text
is schema:about of	named entity 'improving' named entity 'ER stress' named entity 'PGC-1α' named entity 'level' named entity 'provide' named entity 'IKKβ' named entity 'skeletal muscle' named entity 'Objective' named entity 'NFκB' named entity 'IKKβ' named entity 'ER stress' named entity 'improved' named entity 'mitochondrial' named entity 'accompanied' named entity 'regulates' named entity 'investigated' named entity 'ER stress' named entity 'function' named entity 'ACE2' named entity 'ACE2' named entity 'ACE2' named entity 'mitochondrial' named entity 'reduced' named entity 'ACE2' named entity 'ER stress' named entity 'lipid' named entity 'knockout mice' named entity 'IRS-1' named entity 'detected' named entity 'stress' named entity 'NFκB' named entity 'skeletal muscle' named entity 'skeletal muscle' named entity 'skeletal muscle' named entity 'insulin resistance' named entity 'lipid metabolism' named entity 'skeletal muscle' named entity 'skeletal muscle' named entity 'mitochondrial function' named entity 'mice' named entity 'IRS-1' named entity 'knockout mice' named entity 'skeletal muscle' named entity 'Angiotensin-converting enzyme 2' named entity 'skeletal muscle' named entity 'triglycerides' named entity 'mice' named entity 'ACE2' named entity 'IRE1α' named entity 'long-chain fatty acids' named entity 'skeletal muscle' named entity 'XBP-1' named entity 'substrates' named entity 'SDHB' named entity 'IKKβ' named entity 'gastrocnemius muscle' named entity 'IRS-1' named entity 'ACE2' named entity 'mRNA' named entity 'UPR' named entity 'Muscle' named entity 'NFκB' named entity 'GFP' named entity 'nonfat' named entity 'protein' named entity 'real-time PCR' named entity 'PCR' named entity 'acetyl-CoA carboxylase' named entity 'mice' named entity 'down-regulation' named entity 'muscle tissue' named entity 'liver' named entity 'acetyl-CoA'

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