Allgemeine morphologische Pathologie des Cytoplasmas. Die Pathobiosen

Altmann, H. W.

doi:10.1007/978-3-642-86043-0_9

Cited by 30 publications

(2 citation statements)

References 760 publications

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“…ER, mitochondria, and other subcellular organelles were mostly seen within single (rarely double)-membrane organelles that were called “cytolysomes” ( 35 ) or autophagic vacuoles ( 8 ). Analysis of the micrographs immediately raised questions such as “how do organelles get access to the lumen of degradative compartments?” and “are organelles selectively or nonselectively taken up by degradative compartments?” ( 7 , 8 , 34 , 36 ).…”

Section: Introductionmentioning

confidence: 99%

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Reggiori

Molinari

2022

Physiological Reviews

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ER-phagy (reticulo-phagy) defines the degradation of portions of the endoplasmic reticulum (ER) within lysosomes or vacuoles. It is part of the self-digestion (i.e., auto-phagic) programs recycling cytoplasmic material and organelles, which rapidly mobilize metabolites in cells confronted with nutrient shortage. Moreover, selective clearance of ER subdomains participates to the control of ER size and activity during ER stress, the re-establishment of ER homeostasis after ER stress resolution and the removal of ER parts, in which aberrant and potentially cytotoxic material has been segregated. ER-phagy relies on the individual and/or concerted activation of the ER-phagy receptors, ER peripheral or integral membrane proteins that share the presence of LC3/Atg8-binding motifs in their cytosolic domains. ER-phagy involves the physical separation of portions of the ER from the bulk ER network, and their delivery to the endolysosomal/vacuolar catabolic district. This last step is accomplished by a variety of mechanisms including macro-ER-phagy (in which ER fragments are sequestered by double-membrane autophagosomes that eventually fuse with lysosomes/vacuoles), micro-ER-phagy (in which ER fragments are directly engulfed by endosomes/lysosomes/vacuoles), or direct fusion of ER-derived vesicles with lysosomes/vacuoles. ER-phagy is dysfunctional in specific human diseases and its regulators are subverted by pathogens, highlighting its crucial role for cell and organism life.

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Section: Introductionmentioning

confidence: 99%

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Reggiori

Molinari

2022

Physiological Reviews

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“…At least some of the mechanistic considerations by Karbe and Kerlin remain inconclusive. The ambiguity of the term degeneration has already been realized in the early 1950s by Altman (10). More recently, Majno and Joris (11) stated that "the term degeneration was widely used in pathology before the 1950s when little was known in cell biology; it vaguely implied that some sort of breakdown was involved," but "today we know better," and should restrict the ".…”

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confidence: 99%

Comments on R. Karbe and R. L. Kerlin (2002). Cystic Degeneration/Spongiosis Hepatis (Toxicol Pathol 30 (2), 216—227) PETER BANNASCH

Bannasch¹

2003

Toxicol Pathol

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Karbe and Kerlin have questioned the classification of spongiosis hepatis as a preneoplastic lesion or even a benign neoplasm, designated as spongiotic pericytoma, and have proposed to use the term cystic degeneration for this lesion in rats and fish. However, the reclassification of spongiosis as cystic degeneration is unwarranted for several reasons. In the rat, spongiosis hepatis represents a specific pathomorphologic entity, originating from the perisinusoidal (Ito) cells; it may occur spontaneously in aged animals but its number and size increases significantly after exposure to various (hepato)carcinogens. Comparative morphological, immunohistochemical, and autoradiographic studies in rats exposed to N-nitrosomorpholine revealed that spongiosis hepatis is an integral part of larger proliferative Ito-cell aggregates showing an autonomous, progressive growth. The classification of spongiosis hepatis as a benign neoplasm is based on these findings that endorse and extend previous considerations on the preneoplastic or neoplastic nature of this lesion. Irrespective of the classification of spongiosis hepatis as a benign neoplastic or a preneoplastic lesion, there is compelling evidence for its reliability as a sensitive marker for (hepato)carcinogenic effects in rats and fish. The data collected by Karbe and Kerlin support rather than contradict the reliability of spongiosis hepatis as an effect marker for carcinogens.Keywords. Spongiosis hepatis; spongiotic pericytoma; perisinusoidal (Ito) cell neoplasm; perisinusoidal cell sarcoma; effect marker for (hepato) carcinogens.In their communication Karbe and Kerlin question the classification of spongiosis hepatis as a putative preneoplastic lesion (1, 2) or even a benign neoplasm (spongiotic pericytoma) in rat (3), and fish (4), and propose to use the term cystic degeneration for this lesion. The authors do not present any new data but base their proposal on a review of most, albeit not all, of the available literature. A reclassification of spongiosis hepatis as cystic degeneration, a term previously recommended in some diagnostic guidelines (eg, 5, 6), is unwarranted for several reasons.Karbe and Kerlin argue that the morphology of cystic degeneration/spongiosis hepatis "does not have standard neoplastic characteristics." For this reason the term spongiosis hepatis originally coined and introduced into the literature was deliberately descriptive (1). Nevertheless, a preneoplastic or neoplastic nature of spongiosis hepatis has been considered since its first description, which was exclusively based on morphologic criteria in both rats and fish (1, 2, 4, 7). Light and electron microscopic observations in these species revealed that spongiosis hepatis represents a specific pathomorphologic entity originating from the perisinusoidal (Ito) cells. This histogenetic relationship has been substantiated by the selective immunohistochemical demonstration of desmin (Figure 1) in both normal perisinusoidal liver cells and cells constituting spongiosis hepatis (3).T...

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Persisting Structural Abnormalities in Liver, Kidney, and Muscle Tissues Following Hemorrhagic Shock

George¹,

Ryan²,

Ullrick³

et al. 1978

Arch Surg

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Allgemeine morphologische Pathologie des Cytoplasmas. Die Pathobiosen

Cited by 30 publications

References 760 publications

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum

Comments on R. Karbe and R. L. Kerlin (2002). Cystic Degeneration/Spongiosis Hepatis (Toxicol Pathol 30 (2), 216—227) PETER BANNASCH

Persisting Structural Abnormalities in Liver, Kidney, and Muscle Tissues Following Hemorrhagic Shock

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