Exploring the contribution of the mitochondrial disulfide relay system to Parkinson's disease: The PINK1/CHCHD4 interplay

Giuseppe Arena; Nazanine Modjtahedi; Rejko Kruger

doi:10.4103/1673-5374.310679

Exploring the contribution of the mitochondrial disulfide relay system to Parkinson's disease: The PINK1/CHCHD4 interplay

Giuseppe Arena^*, Nazanine Modjtahedi, Rejko Kruger

^*Corresponding author for this work

Transversal Translational Medicine

Research output: Contribution to journal › Review article › peer-review

6 Citations (Scopus)

Original language	English
Pages (from-to)	2222-2224
Number of pages	3
Journal	Neural Regeneration Research
Volume	16
Issue number	11
DOIs	https://doi.org/10.4103/1673-5374.310679
Publication status	Published - Nov 2021

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10.4103/1673-5374.310679Licence: CC BY-NC-SA

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@article{9b4327bc7144440f89edb33ea6028c5b,

title = "Exploring the contribution of the mitochondrial disulfide relay system to Parkinson's disease: The PINK1/CHCHD4 interplay",

author = "Giuseppe Arena and Nazanine Modjtahedi and Rejko Kruger",

note = "Funding Information: findings revealed that, upon binding to human health and disease. J Pathol 241:251-the reduced pyridine nucleotide cofactors Bender A, Krishnan KJ, Morris CM, Taylor GA, 263. nicotinamide adenine dinucleotide (NADH) This work was supported by grants from ?eeve AK 唀 Perry ?H 唀 Jaros E 唀 Hersheson JS 唀 ?etts and nicotinamide adenine dinucleotide the Luxembourg National Research Fund J, Klopstock T, Taylor RW, Turnbull DM (2006) phosphate (NADPH), AIF undergoes 縀FNR 缀 for the National Centre for Excellence High levels of mitochondrial DNA deletions in a conformational modification, which in Research on Parkinson ? s disease 縀NCER ? disease. Nat Genet 38:515-517. substantia nigra neurons in aging and Parkinson appears to enhance its interaction PD to RK 缃唀 the PEARL program 縀FNR ? BrunelliF,Valente EM,ArenaG (2020)Mechanisms with CHCHD4 (Reinhardt et al., 2020). P 氃 to RK? 缀P Da n 縀d MC iRisk? of neurodegeneration in Parkinson ? s disease P Interestingly ? PD 爁?elated mutations in PINBKM ? 氃 to RK and GA 缃堀 RK has also keep neurons in the PINK1. Mech Ageing Dev and GBA genes decreased nicotinamide received research grants from the Michael Gao F, Zhang Y, Hou X, Tao Z, Ren H, Wang G 189:111277. adenine dinucleotide (NAD+) levels, J Fox Foundation 唀 the European Union ? s 縃缀 Dependence of PINK  accumulation leading to mitochondrial dysfunction Joint Program 爀Neurodegenerative Diseases 19:e13211. on mitochondrial redox system. Aging Cell and neurodegeneration. In contrast, 縀JPND 嘀 COURAGE 爀PD 缃唀 the European UImai Ynion 唀 Meng H 唀 Shiba 爀Fuk? s ushima K 唀 Hattori N boosting the intracellular pool of pyridine Horizon  research and innovation (2019) Twin CHCH proteins, CHCHD2, and nucleotide cofactors upon supplementation program 縀No 堀 缃唀 and the Federal CHCHD10: key molecules of Parkinson{\textquoteright}s with the NAD+ precursors Nicotinamide Ministry for Education and Research 縀BMBF 嘀 frontotemporal dementia 堀 Int J Mol Sci P ?disease, amyotrophic lateral sclerosis, and o r Nic o tinamide Ribo side r escued Mito 爀PD  A  A 缃堀 NM was supportKim KHed , Song K, Yoon SH, Shehzad O, Kim YS, mitochondrial defects and neuronal loss in by the French National Cancer Institute Son JH (2012) Rescue of PINK1 protein null-Drosophila and human induced pluripotent 縀INCA 爃爀PLBIO 爃缀 and by Fspecific mitondation ochondrial complex IV deficits stem cells-derived models of PD (Sch{\"o}ndorf pour la recherche contre le cancer 縀ARC 缃? signaling. J Biol Chem 287:44109-44120. by ginsenoside ?e activation of nitric oxide et al., 2018). If this translates in increased Maguire JJ, Tyurina YY, Mohammadyani D, Kapralov AIF/CHCHD4 binding and enhanced CHCHD4 Giuseppe Arena*, AA, Anthonymuthu TS, Qu F, Amoscato AA, activity remains to be demonstrated 唀 as well Nazanine Modjtahedi 唀 Rejko Kruger Klein 爀Seetharaman J唀 ?ayır H 唀 Kagan VE 縃缀 Sparvero LJ, Tyurin VA, Planas-Iglesias J, He RR, as the potential contribution of this pathway Known unknowns of cardiolipin signaling: The Translational Neuroscience group 唀 Luxembourg in the neuroprotective effects of NADof Luxembourg唀 Esch 爁送딁?爀Alzette 唀 LuxembouCell Biol Lipids 1862:8-24.rg +Centre for Systems Biomedicine (LCSB), University best is yet to come. Biochim Biophys Acta Mol precursors. (Arena G, Kruger R) Poewe W, Seppi K, Tanner CM, Halliday GM, Another mechanism underlying regulation Universit{\'e} Paris 爀Saclay唀 Gustave ?oussy Institute 唀 Brundin P, Volkmann J, Schrag AE, Lang AE (2017) of the CHCHD4/GFER disulfide relay system Reinhardt C, Arena G, Nedara K, Edwards R, CNRS, Metabolic and systemic aspects of Parkinson disease. Nat Rev Dis Primers 3:17013. could involve potential post-translational Brenner C, Tokatlidis K, Modjtahedi N (2020) oncogenesis for new therapeutic approaches 唀 modifications of either AIF or CHCHD4, Parkinson Research Clinic, Centre Hospitalier du Villejuif, France (Modjtahedi N) AIF meets the CHCHD4/Mia40-dependent which may control their protein-protein Luxembourg 縀CHL 缃唀 Esch 爁送딁?爀Alzette 唀 LuAxecmtab Mouorl gB asis Dis 1866:165746. mitochondrial import pathway. Biochim Biophys interaction and modulate the activity of (Kruger R) Sch{\"o}ndorf DC, Ivanyuk D, Baden P, Sanchez- AIF/CHCHD4 complex. If PINK1 could play Transversal Translational Medicine 唀 Luxembourg Martinez A 唀 De Cicco S 唀 Yu C 唀 Giunta I 唀 Schwarz a role in that sense, for instance by means Institute of Health 縀LIH 缃唀 Esch 爁送딁?爀Alzette 唀 LK, Di Napoli G, Panagiotakopoulou V, Nestel S, of its kinase activity, still needs further Luxembourg (Kruger R) B, Gasser T, Whitworth AJ, Deleidi M (2018) The Keatinge M 唀 Pruszak J 唀 ?andmann O唀 Heimrich investigation 唀 but distinct observations make *Correspondence to: Giuseppe Arena, PhD, NADA㴀 precursor nicotinamide riboside rescues this possibility worthy of being explored. [email protected]. mitochondrial defects and neuronal loss in iPSC First, PINK1 and CHCHD4 bind to each other 23:2976-2988.https P 氃?orcid 堁紁?g 氃爃爃爃?and fly models of Parkinson ? s disease 堀 Cell ? ep not only in dysfunctional mitochondria, Sekine S, Wang C, Sideris DP, Bunker E, Zhang (Giuseppe Arena) destined to mitophagy, but also in healthy Date of decision: November 13, 2020 Date of submission: October 5, 2020 Z, Youle RJ (2019) Reciprocal roles of Tom7 polarized organelles, thus extending the Date of acceptance: January 18, 2021 activation of PINK 堀 Mol Cell P 爃堁ḃ堀 and OMA1 during mitochondrial import and functional consequences of their interaction Date of web publication P March 25, 2021 Sekine S 唀 Youle J 縃缀 PINK  import r egulation 嘀 behind the simple control of PINK1 a fine system to convey mitochondrial stress to accumulation on the OMM by CHCHD4 https P 氃氁ᨁ紁崃堁紁?g氃堃氃爃堃?the cytosol. BMC Biol 16:2. (Gao et al., 2020). This also highlights the How to cite this article: Arena G 唀 Modjtahedi N 唀",

year = "2021",

month = nov,

doi = "10.4103/1673-5374.310679",

language = "English",

volume = "16",

pages = "2222--2224",

journal = "Neural Regeneration Research",

issn = "1673-5374",

publisher = "Wolters Kluwer Medknow Publications",

number = "11",

}

TY - JOUR

T1 - Exploring the contribution of the mitochondrial disulfide relay system to Parkinson's disease

T2 - The PINK1/CHCHD4 interplay

AU - Arena, Giuseppe

AU - Modjtahedi, Nazanine

AU - Kruger, Rejko

N1 - Funding Information: findings revealed that, upon binding to human health and disease. J Pathol 241:251-the reduced pyridine nucleotide cofactors Bender A, Krishnan KJ, Morris CM, Taylor GA, 263. nicotinamide adenine dinucleotide (NADH) This work was supported by grants from ?eeve AK 唀 Perry ?H 唀 Jaros E 唀 Hersheson JS 唀 ?etts and nicotinamide adenine dinucleotide the Luxembourg National Research Fund J, Klopstock T, Taylor RW, Turnbull DM (2006) phosphate (NADPH), AIF undergoes 縀FNR 缀 for the National Centre for Excellence High levels of mitochondrial DNA deletions in a conformational modification, which in Research on Parkinson ? s disease 縀NCER ? disease. Nat Genet 38:515-517. substantia nigra neurons in aging and Parkinson appears to enhance its interaction PD to RK 缃唀 the PEARL program 縀FNR ? BrunelliF,Valente EM,ArenaG (2020)Mechanisms with CHCHD4 (Reinhardt et al., 2020). P 氃 to RK? 缀P Da n 縀d MC iRisk? of neurodegeneration in Parkinson ? s disease P Interestingly ? PD 爁?elated mutations in PINBKM ? 氃 to RK and GA 缃堀 RK has also keep neurons in the PINK1. Mech Ageing Dev and GBA genes decreased nicotinamide received research grants from the Michael Gao F, Zhang Y, Hou X, Tao Z, Ren H, Wang G 189:111277. adenine dinucleotide (NAD+) levels, J Fox Foundation 唀 the European Union ? s 縃缀 Dependence of PINK  accumulation leading to mitochondrial dysfunction Joint Program 爀Neurodegenerative Diseases 19:e13211. on mitochondrial redox system. Aging Cell and neurodegeneration. In contrast, 縀JPND 嘀 COURAGE 爀PD 缃唀 the European UImai Ynion 唀 Meng H 唀 Shiba 爀Fuk? s ushima K 唀 Hattori N boosting the intracellular pool of pyridine Horizon  research and innovation (2019) Twin CHCH proteins, CHCHD2, and nucleotide cofactors upon supplementation program 縀No 堀 缃唀 and the Federal CHCHD10: key molecules of Parkinson’s with the NAD+ precursors Nicotinamide Ministry for Education and Research 縀BMBF 嘀 frontotemporal dementia 堀 Int J Mol Sci P ?disease, amyotrophic lateral sclerosis, and o r Nic o tinamide Ribo side r escued Mito 爀PD  A  A 缃堀 NM was supportKim KHed , Song K, Yoon SH, Shehzad O, Kim YS, mitochondrial defects and neuronal loss in by the French National Cancer Institute Son JH (2012) Rescue of PINK1 protein null-Drosophila and human induced pluripotent 縀INCA 爃爀PLBIO 爃缀 and by Fspecific mitondation ochondrial complex IV deficits stem cells-derived models of PD (Schöndorf pour la recherche contre le cancer 縀ARC 缃? signaling. J Biol Chem 287:44109-44120. by ginsenoside ?e activation of nitric oxide et al., 2018). If this translates in increased Maguire JJ, Tyurina YY, Mohammadyani D, Kapralov AIF/CHCHD4 binding and enhanced CHCHD4 Giuseppe Arena*, AA, Anthonymuthu TS, Qu F, Amoscato AA, activity remains to be demonstrated 唀 as well Nazanine Modjtahedi 唀 Rejko Kruger Klein 爀Seetharaman J唀 ?ayır H 唀 Kagan VE 縃缀 Sparvero LJ, Tyurin VA, Planas-Iglesias J, He RR, as the potential contribution of this pathway Known unknowns of cardiolipin signaling: The Translational Neuroscience group 唀 Luxembourg in the neuroprotective effects of NADof Luxembourg唀 Esch 爁送딁?爀Alzette 唀 LuxembouCell Biol Lipids 1862:8-24.rg +Centre for Systems Biomedicine (LCSB), University best is yet to come. Biochim Biophys Acta Mol precursors. (Arena G, Kruger R) Poewe W, Seppi K, Tanner CM, Halliday GM, Another mechanism underlying regulation Université Paris 爀Saclay唀 Gustave ?oussy Institute 唀 Brundin P, Volkmann J, Schrag AE, Lang AE (2017) of the CHCHD4/GFER disulfide relay system Reinhardt C, Arena G, Nedara K, Edwards R, CNRS, Metabolic and systemic aspects of Parkinson disease. Nat Rev Dis Primers 3:17013. could involve potential post-translational Brenner C, Tokatlidis K, Modjtahedi N (2020) oncogenesis for new therapeutic approaches 唀 modifications of either AIF or CHCHD4, Parkinson Research Clinic, Centre Hospitalier du Villejuif, France (Modjtahedi N) AIF meets the CHCHD4/Mia40-dependent which may control their protein-protein Luxembourg 縀CHL 缃唀 Esch 爁送딁?爀Alzette 唀 LuAxecmtab Mouorl gB asis Dis 1866:165746. mitochondrial import pathway. Biochim Biophys interaction and modulate the activity of (Kruger R) Schöndorf DC, Ivanyuk D, Baden P, Sanchez- AIF/CHCHD4 complex. If PINK1 could play Transversal Translational Medicine 唀 Luxembourg Martinez A 唀 De Cicco S 唀 Yu C 唀 Giunta I 唀 Schwarz a role in that sense, for instance by means Institute of Health 縀LIH 缃唀 Esch 爁送딁?爀Alzette 唀 LK, Di Napoli G, Panagiotakopoulou V, Nestel S, of its kinase activity, still needs further Luxembourg (Kruger R) B, Gasser T, Whitworth AJ, Deleidi M (2018) The Keatinge M 唀 Pruszak J 唀 ?andmann O唀 Heimrich investigation 唀 but distinct observations make *Correspondence to: Giuseppe Arena, PhD, NADA㴀 precursor nicotinamide riboside rescues this possibility worthy of being explored. [email protected]. mitochondrial defects and neuronal loss in iPSC First, PINK1 and CHCHD4 bind to each other 23:2976-2988.https P 氃?orcid 堁紁?g 氃爃爃爃?and fly models of Parkinson ? s disease 堀 Cell ? ep not only in dysfunctional mitochondria, Sekine S, Wang C, Sideris DP, Bunker E, Zhang (Giuseppe Arena) destined to mitophagy, but also in healthy Date of decision: November 13, 2020 Date of submission: October 5, 2020 Z, Youle RJ (2019) Reciprocal roles of Tom7 polarized organelles, thus extending the Date of acceptance: January 18, 2021 activation of PINK 堀 Mol Cell P 爃堁ḃ堀 and OMA1 during mitochondrial import and functional consequences of their interaction Date of web publication P March 25, 2021 Sekine S 唀 Youle J 縃缀 PINK  import r egulation 嘀 behind the simple control of PINK1 a fine system to convey mitochondrial stress to accumulation on the OMM by CHCHD4 https P 氃氁ᨁ紁崃堁紁?g氃堃氃爃堃?the cytosol. BMC Biol 16:2. (Gao et al., 2020). This also highlights the How to cite this article: Arena G 唀 Modjtahedi N 唀

PY - 2021/11

Y1 - 2021/11

UR - http://www.scopus.com/inward/record.url?scp=85103448832&partnerID=8YFLogxK

UR - https://www.ncbi.nlm.nih.gov/pubmed/33818502

U2 - 10.4103/1673-5374.310679

DO - 10.4103/1673-5374.310679

M3 - Review article

C2 - 33818502

AN - SCOPUS:85103448832

SN - 1673-5374

VL - 16

SP - 2222

EP - 2224

JO - Neural Regeneration Research

JF - Neural Regeneration Research

IS - 11

ER -

Exploring the contribution of the mitochondrial disulfide relay system to Parkinson's disease: The PINK1/CHCHD4 interplay

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