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An alternative explanation is that systemic inflammation may trigger the glycolysis.
In spite of previous hypothesis, early subclinical inflammation may trigger the chronic sequence of kidney fibrosis, resulting in kidney graft failure.
The hypothesis, that inflammation may trigger the development of AF in critically ill patients, is supported by our observation of increasing CRP plasma concentrations before the onset of AF in septic shock patients.
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This local inflammation may trigger a systematic response in the host.
Thus, the milieu of chronic myocardial inflammation may trigger their differentiation not just into adipocytes and myofibroblasts, but also possibly in cells capable of attracting and supporting lymphocytes.
We hypothesize that saturated fat-induced, low-grade muscle cell inflammation may trigger resident skeletal muscle macrophage polarization, possibly contributing to insulin resistance in vivo.
Although the role of BTL maintenance mechanisms in surrogate tissues like blood leukocytes remains largely unexplored in cancer patients, it is biologically plausible that critical BTL shortening (via age or increased oxidative stress or inflammation) may trigger telomere maintenance mechanisms to protect telomere integrity (Hodes et al., 2002).
It is debated whether chronic urogenital inflammations and infections may trigger the formation of antisperm antibodies (ASA) in semen.
4 6 We have shown that hard metal accumulated in the centrilobular area may trigger the inflammation in cooperation with CD163 monocyte-macrophages and CD8 lymphocytes using electron probe microanalysers with a wavelength dispersive spectrometer (EPMA-WDS).
We speculate that an increased TNF α protein levels may trigger the development of allergic inflammation.
Accumulation of mutant TNFR1 in the ER may trigger the ER stress response, which could directly or indirectly lead to inflammation.
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