Matches in SemOpenAlex for { <https://semopenalex.org/work/W2104378453> ?p ?o ?g. }
Showing items 1 to 87 of
87
with 100 items per page.
- W2104378453 endingPage "487" @default.
- W2104378453 startingPage "482" @default.
- W2104378453 abstract "Apoptosis is defined as the process of ''programmed cell death'' (PCD), during which many cells simultaneously die from within along a very orderly pattern. PCD is as intrinsic for cells as mitosis and is involved in both degenerative and developmental processes of organs and organisms. The pattern of apoptotic cell decay is caused by the total cellular content. Since all body cells possess the same genome, they are similar in many aspects and, therefore, the major processes are nearly identical in all cell types. The same destructive processes also occur continuously in healthy living cells, but then the capacity of repair mechanisms is sufficient to effect cellular integrity. Decay processes become visible, as soon as repair can no more be sufficient. PCD starts as soon as produced energy is permanently insufficient to repress decay. Decreased energy production may arise due to (i) turning off the pivotal tricarbonic acid cycle, (ii) turning off oxidative phosphorylation, (iii) damage of mitochondria, and (iv) inhibition of mitochondrial biogenesis regarding both the mitochondrial and the nuclear part. The consequence of this kind of decreased energy production will be a massive, inefficient fermentative energy production with enormous amounts of lactic acid. Increasing acidity and falling pH will slow down enzymatic activities and thus also intracellular processes. As soon as energy for repair has become insufficient, cellular decay becomes irreversible and the cell will die. Thus, the mitochondrial apoptotic pathway is suggested to arise due to low mitochondrial energy production. For optimal functioning cells need adequate internal conditions and cellular morphology. Cellular morphology depends on (i) the intracellular turgor, (ii) the intracellular cytoskeleton, and (iii) close intercellular contact with neighbour cells. Lack of energy implies decrease of turgor and, consequently, a strong decline of conditions needed for adequate functioning of the cell. Thus, if this lack of energy cannot be repaired in time, it will contribute to cellular decay. Various cellular components or systems that are not directly linked to mitochondria, may be functionally inhibited or damaged and thus contribute to apoptosis. These components or systems that probably constitute the non-mitochondrial pathway are (i) the cellular uptake systems for energy-rich substrates, (ii) extra-mitochondrial enzymes that are involved in non-mitochondrial processes of oxidative energy production, (iii) cytoplasmatic, non-mitochondrial protein synthesis, (iv) the system that regulates osmotic conditions and turgor, and (v) the synthesis and repair of the cytoskeleton. After this careful reflection I am convinced that apoptosis is merely the complex machinery of cellular decay after energy generation has irreversibly stopped. Therefore, apoptosis research for health care should be focussed on processes that hinder energy production. For therapeutic aims research should be focussed on metabolic aspects of energy production and on mitochondrial processes." @default.
- W2104378453 created "2016-06-24" @default.
- W2104378453 creator A5035223108 @default.
- W2104378453 date "2008-01-01" @default.
- W2104378453 modified "2023-09-25" @default.
- W2104378453 title "What of apoptosis is important: The decay process or the causative origin?" @default.
- W2104378453 cites W1507812324 @default.
- W2104378453 cites W1518531052 @default.
- W2104378453 cites W1532194993 @default.
- W2104378453 cites W1535426243 @default.
- W2104378453 cites W1572252257 @default.
- W2104378453 cites W1591646293 @default.
- W2104378453 cites W1606295911 @default.
- W2104378453 cites W1982549933 @default.
- W2104378453 cites W2023509911 @default.
- W2104378453 cites W2037159578 @default.
- W2104378453 cites W2042345167 @default.
- W2104378453 cites W2047453903 @default.
- W2104378453 cites W2050528738 @default.
- W2104378453 cites W2050866010 @default.
- W2104378453 cites W2060270769 @default.
- W2104378453 cites W2068005505 @default.
- W2104378453 cites W2085979150 @default.
- W2104378453 cites W2090466136 @default.
- W2104378453 cites W2091493364 @default.
- W2104378453 cites W2170926992 @default.
- W2104378453 doi "https://doi.org/10.1016/j.mehy.2007.07.006" @default.
- W2104378453 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17728070" @default.
- W2104378453 hasPublicationYear "2008" @default.
- W2104378453 type Work @default.
- W2104378453 sameAs 2104378453 @default.
- W2104378453 citedByCount "11" @default.
- W2104378453 countsByYear W21043784532012 @default.
- W2104378453 countsByYear W21043784532017 @default.
- W2104378453 countsByYear W21043784532018 @default.
- W2104378453 countsByYear W21043784532020 @default.
- W2104378453 countsByYear W21043784532022 @default.
- W2104378453 crossrefType "journal-article" @default.
- W2104378453 hasAuthorship W2104378453A5035223108 @default.
- W2104378453 hasConcept C104317684 @default.
- W2104378453 hasConcept C131934819 @default.
- W2104378453 hasConcept C1491633281 @default.
- W2104378453 hasConcept C190283241 @default.
- W2104378453 hasConcept C2777229759 @default.
- W2104378453 hasConcept C28859421 @default.
- W2104378453 hasConcept C31573885 @default.
- W2104378453 hasConcept C55493867 @default.
- W2104378453 hasConcept C57600042 @default.
- W2104378453 hasConcept C79879829 @default.
- W2104378453 hasConcept C86803240 @default.
- W2104378453 hasConcept C93304396 @default.
- W2104378453 hasConcept C95444343 @default.
- W2104378453 hasConceptScore W2104378453C104317684 @default.
- W2104378453 hasConceptScore W2104378453C131934819 @default.
- W2104378453 hasConceptScore W2104378453C1491633281 @default.
- W2104378453 hasConceptScore W2104378453C190283241 @default.
- W2104378453 hasConceptScore W2104378453C2777229759 @default.
- W2104378453 hasConceptScore W2104378453C28859421 @default.
- W2104378453 hasConceptScore W2104378453C31573885 @default.
- W2104378453 hasConceptScore W2104378453C55493867 @default.
- W2104378453 hasConceptScore W2104378453C57600042 @default.
- W2104378453 hasConceptScore W2104378453C79879829 @default.
- W2104378453 hasConceptScore W2104378453C86803240 @default.
- W2104378453 hasConceptScore W2104378453C93304396 @default.
- W2104378453 hasConceptScore W2104378453C95444343 @default.
- W2104378453 hasIssue "3" @default.
- W2104378453 hasLocation W21043784531 @default.
- W2104378453 hasLocation W21043784532 @default.
- W2104378453 hasOpenAccess W2104378453 @default.
- W2104378453 hasPrimaryLocation W21043784531 @default.
- W2104378453 hasRelatedWork W2030811002 @default.
- W2104378453 hasRelatedWork W2080270879 @default.
- W2104378453 hasRelatedWork W2099913917 @default.
- W2104378453 hasRelatedWork W2170804462 @default.
- W2104378453 hasRelatedWork W2366219004 @default.
- W2104378453 hasRelatedWork W2378071104 @default.
- W2104378453 hasRelatedWork W2558846435 @default.
- W2104378453 hasRelatedWork W2611142423 @default.
- W2104378453 hasRelatedWork W3162789962 @default.
- W2104378453 hasRelatedWork W4200625146 @default.
- W2104378453 hasVolume "70" @default.
- W2104378453 isParatext "false" @default.
- W2104378453 isRetracted "false" @default.
- W2104378453 magId "2104378453" @default.
- W2104378453 workType "article" @default.