Περίληψη:
Tissue hypoxia occurs in various conditions such as myocardial or brain
ischemia and infarction, sepsis, and trauma, and induces cellular damage
and tissue remodeling with recapitulation of fetal-like reprogramming,
which eventually results in organ failure. Analogies seem to exist
between the damaged hypoxic and developing organs, indicating that a
regulatory network which drives embryonic organ development may control
aspects of heart (or tissue) repair. In this context, thyroid hormone
(TH), which is a critical regulator of organ maturation, physiologic
angiogenesis, and mitochondrial biogenesis during fetal development, may
be of important physiological relevance upon stress (hypoxia)-induced
fetal reprogramming. TH signaling has been implicated in hypoxic tissue
remodeling after myocardial infarction and T3 prevents remodeling of the
postinfarcted heart. Similarly, preliminary experimental evidence
suggests that T3 can prevent early tissue hypoxia during sepsis with
important physiological consequences. Thus, based on common pathways
between different paradigms, we propose a possible role of TH in tissue
hypoxia after sepsis with the potential to reduce secondary organ
failure.
Συγγραφείς:
Lourbopoulos, Athanasios I.
Mourouzis, Iordanis S.
Trikas,
Athanasios G.
Tseti, Ioulia K.
Pantos, Constantinos I.
