FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2897626257> ?p ?o ?g. }

• W2897626257 abstract "Objective Myostatin (MSTN) is a member of the TGF-β superfamily and is a negative regulator of skeletal muscle growth. MSTN is also expressed in other tissues such as heart and fat. The purpose of this study was to elucidate the occurrence of myocardial IR caused by myocardial MSTN expression, and to elucidate the regulation of MSTN expression by exercise and improve myocardial IR status and myocardial interstitial fibrosis.&#x0D; Methods The literatures on exercise, myocardial IR, and myocardial MSTN published in recent years were reviewed and summarized.&#x0D; Results 1.Myostatin, which is rarely expressed in myocardium under normal conditions, the appropriate amount of MSTN expression has anti-cardiac hypertrophy, and excessive MSTN expression can cause various cardiovascular diseases. In the IR state, the expression of myocardial inflammatory factors is increased, and MSTN is highly expressed. MSTN acts on the myocardium through various pathways, leading to the occurrence of myocardial fibrosis. In the IR state, possible pathways for inducing high expression of MSTN include: (1) inflammatory factor TNF-α is elevated, and MSTN expression is induced by P38MAPK and NF-KB; (2) The transcription factor Smad-2/3/4 up-regulates the MSTN promoter activity; (3) Glucocorticoid up-regulates MSTN expression; (4) IGF-1 up-regulates MSTN expression via p38MAPK and transcription factor MEF-2; (5) AngII up-regulates MSTN via Ang1 receptor, p38MAPK and MEF-2;(6) urotensin-II and urocortin can stimulate MSTN expression;(7) The ERK-1/2-MEF-2 pathway up-regulates MSTN expression. 3. Possible pathways by which MSTN acts on the myocardium include:(1) MSTN induces Smad2/3 overexpression; (2) MSTN activates the NF-KB pathway; (3) MSTN activates miR-1 expression, inhibits HSP70, and decreases pAkt levels; (4) MSTN inhibits the PI3K-Akt pathway, leading to induction or damage of the downstream pathway. Regular endurance exercise and resistance exercise improve myocardial IR and myocardial interstitial fibrosis involved in MSTN. This effect is mainly dependent on exercise can effectively improve the body's chronic inflammatory state, down-regulate the MSTN superior inducer, resulting in a series of cascade reactions.&#x0D; Conclusions 1.MSTN expression in myocardial tissue is dose-dependent,proper expression of MSTN in the myocardium can prevent cardiac hypertrophy, and overexpression of MSTN can lead to various cardiovascular diseases. 2.Under the hyperglycemia and inflammation state, it can induce high expression of MSTN. After high expression of myocardial MSTN, it can participate in myocardial IR and can lead to myocardial interstitial fibrosis. 3. Exercise can effectively improve the chronic inflammatory state of the body, down-regulate the level of MSTN induction, improve myocardial IR status and IR-induced myocardial interstitial fibrosis.&#x0D;" @default.
• W2897626257 created "2018-10-26" @default.
• W2897626257 creator A5017579714 @default.
• W2897626257 creator A5066285868 @default.
• W2897626257 date "2018-10-04" @default.
• W2897626257 modified "2023-09-24" @default.
• W2897626257 title "PO-273 Exercise, myocardial insulin resistance and myostatin" @default.
• W2897626257 doi "https://doi.org/10.14428/ebr.v1i5.11223" @default.
• W2897626257 hasPublicationYear "2018" @default.
• W2897626257 type Work @default.
• W2897626257 sameAs 2897626257 @default.
• W2897626257 citedByCount "0" @default.
• W2897626257 crossrefType "journal-article" @default.
• W2897626257 hasAuthorship W2897626257A5017579714 @default.
• W2897626257 hasAuthorship W2897626257A5066285868 @default.
• W2897626257 hasBestOaLocation W28976262571 @default.
• W2897626257 hasConcept C104317684 @default.
• W2897626257 hasConcept C118131993 @default.
• W2897626257 hasConcept C126322002 @default.
• W2897626257 hasConcept C134018914 @default.
• W2897626257 hasConcept C167414201 @default.
• W2897626257 hasConcept C2777488582 @default.
• W2897626257 hasConcept C2781080636 @default.
• W2897626257 hasConcept C54355233 @default.
• W2897626257 hasConcept C71924100 @default.
• W2897626257 hasConcept C86339819 @default.
• W2897626257 hasConcept C86803240 @default.
• W2897626257 hasConceptScore W2897626257C104317684 @default.
• W2897626257 hasConceptScore W2897626257C118131993 @default.
• W2897626257 hasConceptScore W2897626257C126322002 @default.
• W2897626257 hasConceptScore W2897626257C134018914 @default.
• W2897626257 hasConceptScore W2897626257C167414201 @default.
• W2897626257 hasConceptScore W2897626257C2777488582 @default.
• W2897626257 hasConceptScore W2897626257C2781080636 @default.
• W2897626257 hasConceptScore W2897626257C54355233 @default.
• W2897626257 hasConceptScore W2897626257C71924100 @default.
• W2897626257 hasConceptScore W2897626257C86339819 @default.
• W2897626257 hasConceptScore W2897626257C86803240 @default.
• W2897626257 hasLocation W28976262571 @default.
• W2897626257 hasOpenAccess W2897626257 @default.
• W2897626257 hasPrimaryLocation W28976262571 @default.
• W2897626257 hasRelatedWork W1779480512 @default.
• W2897626257 hasRelatedWork W1981654342 @default.
• W2897626257 hasRelatedWork W2009571461 @default.
• W2897626257 hasRelatedWork W2028966038 @default.
• W2897626257 hasRelatedWork W2066838079 @default.
• W2897626257 hasRelatedWork W2096209924 @default.
• W2897626257 hasRelatedWork W2127318580 @default.
• W2897626257 hasRelatedWork W2165997106 @default.
• W2897626257 hasRelatedWork W2185328935 @default.
• W2897626257 hasRelatedWork W2514241645 @default.
• W2897626257 isParatext "false" @default.
• W2897626257 isRetracted "false" @default.
• W2897626257 magId "2897626257" @default.
• W2897626257 workType "article" @default.