Bloodletting Acupuncture at Jing-Well Points Alleviates Myocardial Injury in Acute Altitude Hypoxic Rats by Activating HIF-1α/BNIP3 Signaling-Mediated Mitochondrial Autophagy and Decreasing Oxidative Stress

Wang, Chao; Li, Mengxin; Li, Yun-di; Li, Yongping

doi:10.1007/s11655-022-3626-4

Cited by 3 publications

(1 citation statement)

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“…Receptor-dependent mitophagy mechanisms involve mitochondrial outer membrane proteins, such as BNIP3, NIX, and FUN14 domain containing 1 (FUNDC1), which act as inducible receptors upon stimuli like hypoxia and starvation ( Liu et al, 2012 ; Madhu et al, 2020 ; Lampert et al, 2019 ) ( Figure 3 ). Under hypoxia, HIF-1α-induced BNIP3 promotes mitophagy, protecting against renal and myocardial ischemia-reperfusion injury ( Wang et al, 2023 ; Zhang et al, 2019 ; Fu et al, 2020 ; Yang et al, 2019 ). Thus, mitophagy induced by hypoxia is an adaptive metabolic response that prevents increased ROS and cell death ( Zhang et al, 2008 ).…”

Section: The Role Of Hypoxia-induced Mitochondrial Dysregulation In Hphmentioning

confidence: 99%

Mitochondria in hypoxic pulmonary hypertension, roles and the potential targets

Geng

Zhang

et al. 2023

Front. Physiol.

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Mitochondria are the centrol hub for cellular energy metabolisms. They regulate fuel metabolism by oxygen levels, participate in physiological signaling pathways, and act as oxygen sensors. Once oxygen deprived, the fuel utilizations can be switched from mitochondrial oxidative phosphorylation to glycolysis for ATP production. Notably, mitochondria can also adapt to hypoxia by making various functional and phenotypes changes to meet the demanding of oxygen levels. Hypoxic pulmonary hypertension is a life-threatening disease, but its exact pathgenesis mechanism is still unclear and there is no effective treatment available until now. Ample of evidence indicated that mitochondria play key factor in the development of hypoxic pulmonary hypertension. By hypoxia-inducible factors, multiple cells sense and transmit hypoxia signals, which then control the expression of various metabolic genes. This activation of hypoxia-inducible factors considered associations with crosstalk between hypoxia and altered mitochondrial metabolism, which plays an important role in the development of hypoxic pulmonary hypertension. Here, we review the molecular mechanisms of how hypoxia affects mitochondrial function, including mitochondrial biosynthesis, reactive oxygen homeostasis, and mitochondrial dynamics, to explore the potential of improving mitochondrial function as a strategy for treating hypoxic pulmonary hypertension.

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