Matches in SemOpenAlex for { <https://semopenalex.org/work/W4313011447> ?p ?o ?g. }
Showing items 1 to 56 of
56
with 100 items per page.
- W4313011447 abstract "Cardiac myocytes require large amounts of energy generated by mitochondria to sustain contraction, and there is a strong link between mitochondrial dysfunction and heart disease. Defective mitochondria are less efficient at generating ATP, produce excessive reactive oxygen species, and release pro-apoptotic proteins, all of which can lead to loss of cardiac myocytes and reduced ability to sustain contractile function. Therefore, mitochondrial quality control is critical in preventing mitochondria from causing harm to the cell. Selective autophagy of the mitochondria (mitophagy) is the primary mechanism responsible for eliminating dysfunctional mitochondria. Despite intense research focus on mitophagy over the past decade, little is still known about early events in the pathway, and the signals that orchestrate the selective recruitment of the autophagic machinery to dysfunctional mitochondria are unclear. It is known that autophagosome formation requires Atg9, which is embedded in small Golgi-derived vesicles. To date, most data on Atg9 are from yeast and our knowledge of mammalian Atg9a and Atg9b functions in cells and tissues are still limited. Here, we found that Atg9a and Atg9b are expressed in the heart and that both proteins are increased in the infarct border zone after ligation of the LAD. We also discovered that Atg9a and Atg9b are present on distinct vesicles in myocytes. Atg9b-positive vesicles are localized throughout the cytosol, whereas Atg9a-positive vesicles are associated with the mitochondria even under basal conditions. This suggests that they might have distinct functions and that Atg9a may play a more selective role at the mitochondria. Interestingly, Atg9a, but not Atg9b, is degraded by the proteasome upon activation of mitophagy, a potential indication that this may be a mechanism to prevent excessive mitophagy. Overall, our findings suggest that Atg9a and Atg9b play distinct roles in autophagy and mitophagy and that the mitochondrial localization of Atg9a allows it to initiate autophagosome formation more efficiently during mitophagy." @default.
- W4313011447 created "2023-01-05" @default.
- W4313011447 creator A5010754242 @default.
- W4313011447 creator A5054452204 @default.
- W4313011447 creator A5061473222 @default.
- W4313011447 creator A5067352271 @default.
- W4313011447 creator A5067637611 @default.
- W4313011447 date "2022-08-05" @default.
- W4313011447 modified "2023-10-14" @default.
- W4313011447 title "Abstract P2080: Role Of Atg9 Proteins In Regulating Autophagosome Formation" @default.
- W4313011447 doi "https://doi.org/10.1161/res.131.suppl_1.p2080" @default.
- W4313011447 hasPublicationYear "2022" @default.
- W4313011447 type Work @default.
- W4313011447 citedByCount "0" @default.
- W4313011447 crossrefType "journal-article" @default.
- W4313011447 hasAuthorship W4313011447A5010754242 @default.
- W4313011447 hasAuthorship W4313011447A5054452204 @default.
- W4313011447 hasAuthorship W4313011447A5061473222 @default.
- W4313011447 hasAuthorship W4313011447A5067352271 @default.
- W4313011447 hasAuthorship W4313011447A5067637611 @default.
- W4313011447 hasConcept C168296220 @default.
- W4313011447 hasConcept C190283241 @default.
- W4313011447 hasConcept C203522944 @default.
- W4313011447 hasConcept C207200792 @default.
- W4313011447 hasConcept C2779324830 @default.
- W4313011447 hasConcept C28859421 @default.
- W4313011447 hasConcept C55493867 @default.
- W4313011447 hasConcept C86803240 @default.
- W4313011447 hasConcept C95444343 @default.
- W4313011447 hasConceptScore W4313011447C168296220 @default.
- W4313011447 hasConceptScore W4313011447C190283241 @default.
- W4313011447 hasConceptScore W4313011447C203522944 @default.
- W4313011447 hasConceptScore W4313011447C207200792 @default.
- W4313011447 hasConceptScore W4313011447C2779324830 @default.
- W4313011447 hasConceptScore W4313011447C28859421 @default.
- W4313011447 hasConceptScore W4313011447C55493867 @default.
- W4313011447 hasConceptScore W4313011447C86803240 @default.
- W4313011447 hasConceptScore W4313011447C95444343 @default.
- W4313011447 hasIssue "Suppl_1" @default.
- W4313011447 hasLocation W43130114471 @default.
- W4313011447 hasOpenAccess W4313011447 @default.
- W4313011447 hasPrimaryLocation W43130114471 @default.
- W4313011447 hasRelatedWork W156418324 @default.
- W4313011447 hasRelatedWork W1967888239 @default.
- W4313011447 hasRelatedWork W1977930150 @default.
- W4313011447 hasRelatedWork W1993424978 @default.
- W4313011447 hasRelatedWork W2035756758 @default.
- W4313011447 hasRelatedWork W2080168607 @default.
- W4313011447 hasRelatedWork W2506505475 @default.
- W4313011447 hasRelatedWork W2543989099 @default.
- W4313011447 hasRelatedWork W3094078064 @default.
- W4313011447 hasRelatedWork W3175617079 @default.
- W4313011447 hasVolume "131" @default.
- W4313011447 isParatext "false" @default.
- W4313011447 isRetracted "false" @default.
- W4313011447 workType "article" @default.