Homeostasis and evolution in relation to regeneration and repair

Abstract

Homeostasis constitutes a key concept in physiology and refers to self‐regulating processes that maintain internal stability when adjusting to changing external conditions. It diminishes internal entropy constituting a driving force behind evolution. Natural selection might act on homeostatic regulatory mechanisms and control mechanisms including homeodynamics, allostasis, hormesis and homeorhesis, where different stable stationary states are reached. Regeneration is under homeostatic control through hormesis. Damage to tissues initiates a response to restore the impaired equilibrium caused by mild stress using cell proliferation, cell differentiation and cell death to recover structure and function. Repair is a homeorhetic change leading to a new stable stationary state with decreased functionality and fibrotic scarring without reconstruction of the 3‐D pattern. Mechanisms determining entrance of the tissue or organ to regeneration or repair include the balance between innate and adaptive immune cells in relation to cell plasticity and stromal stem cell responses, and redox balance. The regenerative and reparative capacities vary in different species, distinct tissues and organs, and at different stages of development including ageing. Many cell signals and pathways play crucial roles determining regeneration or repair by regulating protein synthesis, cellular growth, inflammation, proliferation, autophagy, lysosomal function, metabolism and metalloproteinase cell signalling. Attempts to favour the entrance of damaged tissues to regeneration in those with low proliferative rates have been made; however, there are evolutionary constraint mechanisms leading to poor proliferation of stem cells in unfavourable environments or tumour development. More research is required to better understand the regulatory processes of these mechanisms. image

Fried Soybean Oil Causes Systemic Low-Grade Inflammation by Disrupting the Balance of Gut Microbiota in Mice

“…Within a certain range, increasing exposure levels may attenuate, rather than enhance, the strength of an organism’s response, reflecting the complex regulatory mechanisms in the body, including adaptive responses and negative feedback inhibitory pathways [ 33 ]. For example, initial exposure to low doses of fried oil may stimulate a rapid TNF-α response; however, the subsequent activation of negative feedback mechanisms may have led to a decrease in its levels at the time point of our observations [ 34 ]. In addition, our study focuses on short-term exposure effects, where organisms may utilize adaptive mechanisms to respond effectively to such inflammatory stimuli, explaining the observation of a short-term decline in TNF-α.…”