The VIII International Congress on Stress Proteins in Biology and Medicine: täynnä henkeä

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We present new data on the effects of HBOT on human kidney (HK-2) cell metabolism using a SeaHorse XF Analyzer to evaluate separately the state of mitochondrial and glycolytic energy metabolism. The data are discussed in the context of the concept of cellular caloristasis networks. The information on the changes in cellular energy metabolism stimulated by HBOT presented here provides new insights into the cellular energy state and mitochondrial environment in which sHSPs function. These data will be useful in forming testable hypotheses about the functions of translocated sHSPs in human mitochondria responding to stressors.

Section: Hbot and The Caloristasis Networkmentioning

confidence: 97%

The effect of hyperbaric oxygen on mitochondrial and glycolytic energy metabolism: the caloristasis concept

Tezgin

Giardina

Perdrizet

et al. 2020

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“…The fact that small HSP chaperone activity does not require ATP might become extremely important under conditions of energy deprivation and upon stress conditions, when cells need to prioritize use the energy towards cell stress response/ adaptation and survival. The term caloristasis has been coined to complement proteostasis and these are considered as two critical components of cellular metabolic homeostasis (Bonorino et al 2018). Caloristasis, a concept that emphasizes the integrative regulatory interactions needed to understand cellular energy homeostasis, is discussed in more detail in the chapter herein by Tezgin et al Against this background, the ATP-independent chaperone functions of small HSPs during periods of depleted cellular energy reserves take on even greater significance.…”

Section: Hsps and Small Hspsmentioning

confidence: 99%

Studying heat shock proteins through single-molecule mechanical manipulation

Choudhary

Mediani

Carra

et al. 2020

Imbalances of cellular proteostasis are linked to ageing and human diseases, including neurodegenerative and neuromuscular diseases. Heat shock proteins (HSPs) and small heat shock proteins (sHSPs) together form a crucial core of the molecular chaperone family that plays a vital role in maintaining cellular proteostasis by shielding client proteins against aggregation and misfolding. sHSPs are thought to act as the first line of defence against protein unfolding/misfolding and have been suggested to act as "sponges" that rapidly sequester these aberrant species for further processing, refolding, or degradation, with the assistance of the HSP70 chaperone system. Understanding how these chaperones work at the molecular level will offer unprecedented insights for their manipulation as therapeutic avenues for the treatment of ageing and human disease. The evolution in single-molecule force spectroscopy techniques, such as optical tweezers (OT) and atomic force microscopy (AFM), over the last few decades have made it possible to explore at the single-molecule level the structural dynamics of HSPs and sHSPs and to examine the key molecular mechanisms underlying their chaperone activities. In this paper, we describe the working principles of OT and AFM and the experimental strategies used to employ these techniques to study molecular chaperones. We then describe the results of some of the most relevant single-molecule manipulation studies on HSPs and sHSPs and discuss how these findings suggest a more complex physiological role for these chaperones than previously assumed.

“…Changes in mitochondrial function have major consequences for the cell's ability to maintain cellular energy homeostasis. As more metabolomic data begins to emerge through further studies such as those mentioned above and the data presented later in this paper, it may be useful to compile a Bcaloristasis network ( Bonorino et al 2018). There is a critical link between proteostasis and cellular energy homeostasis, as protein metabolism is the most energy-expensive process in most cells (Lindqvist et al 2018).…”

Section: Current Study Datamentioning

confidence: 99%

Might hyperbaric oxygen therapy (HBOT) reduce renal injury in diabetic people with diabetes mellitus? From preclinical models to human metabolomics

Harrison

Giardina

Hightower

et al. 2018

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Diabetic kidney disease (DKD) is the leading cause of end-stage renal failure in the western world. Current treatment of diabetic kidney disease relies on nutritional management and drug therapies to achieve metabolic control. Here, we discuss the potential application of hyperbaric oxygen therapy (HBOT) for the treatment of diabetic kidney disease (DKD), a treatment which requires patients to breathe in 100% oxygen at elevated ambient pressures. HBOT has traditionally been used to diabetic foot ulcers (DFU) refractory to conventional medical treatments. Successful clinic responses seen in the DFU provide the underlying therapeutic rationale for testing HBOT in the setting of DKD. Both the DFU and DKD have microvascular endothelial disease as a common underlying pathologic feature. Supporting evidence for HBOT of DKD comes from previous animal studies and from our preliminary prospective clinical trial reported here. We report urinary metabolomic data obtained from patients undergoing HBOT for DFU, before and after exposure to 6 weeks of HBOT. The preliminary data support the concept that HBOT can reduce biomarkers of renal injury, oxidant stress, and mitochondrial dysfunction in patients receiving HBOT for DFU. Further studies are needed to confirm these initial findings and correlate them with simultaneous measures of renal function. HBOT is a safe and effective treatment for DFU and could also be for individuals with DKD.