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PubMed1977

Histopathology of acute and chronic inflammation.

Inflammation, defined as local reaction to injury, is basically a homeostatic process-loop system with morphological and biochemical components. If this homeostatic loop is uncomplicated a normal situation is reached soon after injury. Morphologically different patterns of inflammation can appear, depending on the character and intensity of the injury. Furthermore, the contributions made by hyperaemia, exudation of fluid, infiltrates carrying inflammatory cells, and cell proliferation not only vary with the type of injury but also depend on the time after injury. Some of the histopathological changes can be seen as essential for the restoration of the normal situation, whereas others damage the tissue more than seems desirable. The morphological aspects of different types of inflammation are discussed in relation to the homeostatic nature of the inflammatory process.

Acute Disease↗
PubMedDate not supplied

Pathogenesis of chronic inflammation in experimental ferritin-induced arthritis. IV. Immuno-electron microscopic techniques in the study of articular collagenous tissues.

The earliest and most severe changes in articular collagenous tissues (ACT) occur within 24 hours of antigen challenge and are associated with and are possibly secondary to maximal immune complex deposition in ACT surfaces. The immuno-electron microscopic (immuno-em) staining characterizes the ferritin as aggregates with antibody and suggests its occurrence and deposition as a preformed immune complex. These data indicate a direct interaction between immune complexes and collagenous matrix which could relate to both antigen persistence and chronicity of the immune response. The changes described in this model have features in common with rheumatoid disease and suggest the potential for similar mechanisms of cartilage degradation.

Animals↗
PubMed2025

Aberrant TERT expression: linking chronic inflammation to hepatocellular carcinoma†.

Telomerase reverse transcriptase (TERT), the catalytic enzyme component of telomerase, plays multiple roles in cellular biology. Its canonical function is primarily associated with telomere maintenance and genomic stability. In addition, several studies revealed critical non-canonical extra-telomeric functions of TERT in various cellular processes, including cell proliferation and survival, DNA damage response, transcription, signal transduction, and metabolic regulation, both in normal and in cancer cells. Notably, TERT is aberrantly upregulated in more than 80% of hepatocellular carcinoma (HCC) cases, making it an important target in liver cancer research. However, due to the diversity and complexity of TERT's functions in vivo, the precise mechanisms by which TERT contributes to the initiation and progression of HCC remain unclear. A recent study published in The Journal of Pathology using the Alb-Cre;TertTg mouse model and clinical HCC samples addresses the role of TERT in hepatocarcinogenesis. The study demonstrates that TERT promotes cell cycle progression and hepatocarcinogenesis by enhancing NF-κB promoter activity and facilitating the ubiquitination of p21. Notably, absence of functional p53 accelerates liver tumor development in TERT transgenic mice. These findings further underscore the critical role of TERT in inflammation-driven hepatocarcinogenesis and provide new insights into its underlying mechanisms. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Telomerase↗