Zhang 2018 Mil Med Res

Zhang H, Feng YW, Yao YM (2018) Potential therapy strategy: targeting mitochondrial dysfunction in sepsis. Mil Med Res 5:41. https://doi.org/10.1186/s40779-018-0187-0

» PMID: 30474573 Open Access

Zhang Hui, Feng Yong-Wen, Yao Yong-Ming (2018) Mil Med Res

Abstract: Recently, the definition of sepsis was concluded to be a life-threatening organ dysfunction caused by a dysregulated host response to infection. Severe patients always present with uncorrectable hypotension or hyperlactacidemia, which is defined as septic shock. The new definition emphasizes dysregulation of the host response and multiple organ dysfunction, which is partially attributed to metabolic disorders induced by energy crisis and oxidative stress. Mitochondria are a cellular organelle that are well known as the center of energy production, and mitochondrial damage or dysfunction is commonly induced in septic settings and is a predominant factor leading to a worse prognosis. In the present review, we determine the major mitochondrial disorders from morphology to functions in sepsis. In the following, several clinical or pre-clinical assays for monitoring mitochondrial function are demonstrated according to accumulated evidence, which is the first step of specific therapy targeting to modulate mitochondrial function. Accordingly, various reagents used for regulating mitochondrial enzyme activities and promoting biogenesis have been documented, among which mitochondria-targeted cation, TPP-conjugated antioxidants are the most valuable for future trials and clinical treatment to improve mitochondrial function as they may take advantage of the prognosis associated with septic complications. • Keywords: Electron transfer chain, Mitochondria, Monitor, Sepsis, Therapy strategy • Bioblast editor: Plangger M

Labels: MiParea: Respiration  Pathology: Sepsis 

Tissue;cell: Blood cells, Platelet 

HRR: Oxygraph-2k 

Labels, 2019-12, CN, MitoEAGLE blood cells reviews 

Correction: FADH₂ and S-pathway

» Complex II ambiguities

A commonly found error on FADH₂ in the S-pathway requires correction. For clarification, see page 48 in Gnaiger (2020)

• Quote (p 48): "The substrate of CII is succinate, which is oxidized forming fumarate while reducing flavin adenine dinucleotide FAD to FADH₂, with further electron transfer to the quinone pool. Whereas reduced NADH is a substrate of Complex I linked to dehydrogenases of the TCA cycle and mt-matrix upstream of CI, reduced FADH₂ is a product of Complex II with downstream electron flow from CII to Q."

Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002