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| Research progress on mitochondrial mechanism of septic cardiomyocytes apoptosis |
| SI Fei1 ZHANG Ling1 LI Pan1 MA Li2 |
1.The Second Clinical Medical College, Lanzhou University, Gansu Province, Lanzhou 730030, China;
2.Department of Emergency ICU， the Second Hospital of Lanzhou University, Gansu Province, Lanzhou 730030, China |
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Abstract Sepsis-induced myocardial dysfunction (SIMD) is the initial cause of multiple organ dysfunction and has always been a difficult point in intensive care unit (ICU) treatment. As the energy factory of cardiomyocytes, mitochondria is involved in occurrence and development of SIMD. And the occurrence of cardiomyocyte apoptosis is closely related to mitochondria. At present, it is believed that the mitochondrial mechanism of cell apoptosis is mainly related to mitochondrial permeablity transition pore (mPTP) opening, mitochondrial respiratory disorder, intracellular Ca2+ overload, mitochondria oxidative/nitrosative stress, caspase family and Bcl-2/Bax apoptosis/inhibition of apoptotic protein release. However, these mechanisms often do not occur independently, but cause and effect each other and promote each other, and eventually induce cardiomyocyte apoptosis, which will lead to or aggravate SIMD. This article will review the mechanism of mitochondria in the apoptosis of sepsis cardiomyocytes, in order to provide a theoretical basis for further research.
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