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Implication of inflammation in pathogenesis of FSGS has been found in some studies [ 29, 30].
With accumulating evidences about the implication of inflammation in the pathogenesis of diseases, the immunoregulatory features of stem cells have drawn more attention.
The association of PTGS2 polymorphism with colorectal cancer points towards the implication of inflammation as an important mediator in the carcinogenesis of these tumours.
In sum, clinical evidence for the implication of inflammation in the development of myocardial hypertrophy and diastolic dysfunction is sparse, although experimental studies suggest a role especially for lymphocytes and macrophages.
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This review summarizes new insights in the pathophysiologic implications of inflammation and microvascular alterations in organ dysfunction, as well as genetic factor contribution, from clinical and experimental studies that were published in 2010 in Critical Care in the fields of multiple organ dysfunction and sepsis.
The cyclooxygenase-2 (COX-2)/prostaglandin E2 pathway in hypoxic cancer cells has important implications for stimulation of inflammation and tumorigenesis.
The systemic implication of sPLA2s in inflammation has prompted a number of research groups to develop selective inhibitors of different types of these enzymes.
The exact cause or implication of the increased inflammation is not clear.
The implication of microscopic follicular inflammation in the pathogenesis of AGA has recently emerged from several independent studies (Jaworsky et al 1992; Whiting 1993; Mahé et al 2000).
Although various extracellular stimuli, including DAMPs, promote tubular inflammation, the implication of intracellular distress processes on tubular inflammation remains to be determined.
These findings have implications for the role of inflammation in cancer progression.
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