Small molecules targeting the NADH-binding pocket of VDAC modulate mitochondrial metabolism in hepatocarcinoma cells

Heslop, Kareem A.; Burger, Pieter B.; Kappler, Christiana S.; Solanki, Ashish K.; Göõz, Monika; Peterson, Yuri K.; Mills, Catherine M.; Benton, Thomas; Duncan, Stephen A.; Woster, Patrick M.; Maldonado, Eduardo N.

doi:10.1016/j.biopha.2022.112928

Cited by 8 publications

(1 citation statement)

References 52 publications

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“…Any change in the cellular dynamic equilibrium activates the synthesis of HSP, including mitochondrial stress ( Minnaar & Szasz, 2022 ). The VDAC control the flux of most anionic respiratory substrates, ATP and small cations across the outer mitochondrial membrane, which is closely related to mitochondrial metabolism ( Heslop et al, 2022 ). PHBs, which are evolutionarily strongly conserved proteins, are able to stabilize mitochondrial translation products ( Aboouf et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Cinnamaldehyde regulates mitochondrial quality against hydrogen peroxide induced apoptosis in mouse lung mesenchymal stem cells via the PINK1/Parkin signaling pathway

Zhu

Lan

et al. 2022

PeerJ

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Background Idiopathic pulmonary fibrosis (IPF) is a fatal respiratory disease without effective treatments. Mitochondrial dysfunction weakens the ability of mesenchymal stem cells (MSCs) to repair the distal lung epithelium, which is a probable pathogenesis of IPF. In previous research, we found that cinnamaldehyde (CA) can maintain the mitochondrial morphology of MSCs. Methods This present study evaluated the effect and mechanism of CA on murine lung MSCs using the hydrogen peroxide model. Antioxidant effects and mitochondrial function were determined using flow cytometry. The mRNA levels of mitochondrial dynamics and the expressions of autophagy-related proteins were also detected. Results CA can increase the levels of SOD, MMP and ATP, decrease the rate of ROS and apoptosis, and restore the mitochondrial structure. CA can also improve the mRNA expression of MFN1, MFN2, FIS1, DRP1, OPA1, and PGC-1α, increase the expression of LC3 II and p62 and promote the PINK1/Parkin signaling pathway. Our results demonstrated that CA can control mitochondrial quality and avoid apoptosis, which may be associated with the regulation of the PINK1/Parkin signaling pathway.

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Section: Discussionmentioning

confidence: 99%