The Interplay between Oxidative Stress and the Nuclear Lamina Contributes to Laminopathies and Age-Related Diseases

被引:10
作者
Kristiani, Lidya [1 ]
Kim, Youngjo [2 ]
机构
[1] Indonesia Int Inst Life Sci, Sch Life Sci, Dept Biomed, Jakarta 13210, Indonesia
[2] Soonchunhyang Univ, Soonchunhyang Inst Medibiosci, Dept Integrated Biomed Sci, Cheonan 31151, South Korea
基金
新加坡国家研究基金会;
关键词
lamins; laminopathy; HGPS; oxidative stress; DNA damage; senescence; aging; DNA-DAMAGE; FARNESYLTRANSFERASE INHIBITOR; STEM-CELLS; PROGERIA; B1; SENESCENCE; A/C; ACCUMULATION; MUTATIONS; ROS;
D O I
10.3390/cells12091234
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Oxidative stress is a physiological condition that arises when there is an imbalance between the production of reactive oxygen species (ROS) and the ability of cells to neutralize them. ROS can damage cellular macromolecules, including lipids, proteins, and DNA, leading to cellular senescence and physiological aging. The nuclear lamina (NL) is a meshwork of intermediate filaments that provides structural support to the nucleus and plays crucial roles in various nuclear functions, such as DNA replication and transcription. Emerging evidence suggests that oxidative stress disrupts the integrity and function of the NL, leading to dysregulation of gene expression, DNA damage, and cellular senescence. This review highlights the current understanding of the interplay between oxidative stress and the NL, along with its implications for human health. Specifically, elucidation of the mechanisms underlying the interplay between oxidative stress and the NL is essential for the development of effective treatments for laminopathies and age-related diseases.
引用
收藏
页数:13
相关论文
共 91 条
  • [1] Mitochondria, oxidants, and aging
    Balaban, RS
    Nemoto, S
    Finkel, T
    [J]. CELL, 2005, 120 (04) : 483 - 495
  • [2] Oxidative stress induces an ATM-independent senescence pathway through p38 MAPK-mediated lamin B1 accumulation
    Barascu, Aurelia
    Le Chalony, Catherine
    Pennarun, Gaelle
    Genet, Diane
    Imam, Naima
    Lopez, Bernard
    Bertrand, Pascale
    [J]. EMBO JOURNAL, 2012, 31 (05) : 1080 - 1094
  • [3] Clinical review: Oxygen as a signaling molecule
    Bartz, Raquel R.
    Piantadosi, Claude A.
    [J]. CRITICAL CARE, 2010, 14 (05):
  • [4] Progerin Expression Induces Inflammation, Oxidative Stress and Senescence in Human Coronary Endothelial Cells
    Bidault, Guillaume
    Garcia, Marie
    Capeau, Jacqueline
    Morichon, Romain
    Vigouroux, Corinne
    Bereziat, Veronique
    [J]. CELLS, 2020, 9 (05)
  • [5] Rapamycin Reverses Cellular Phenotypes and Enhances Mutant Protein Clearance in Hutchinson-Gilford Progeria Syndrome Cells
    Cao, Kan
    Graziotto, John J.
    Blair, Cecilia D.
    Mazzulli, Joseph R.
    Erdos, Michael R.
    Krainc, Dimitri
    Collins, Francis S.
    [J]. SCIENCE TRANSLATIONAL MEDICINE, 2011, 3 (89)
  • [6] Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts
    Cao, Kan
    Blair, Cecilia D.
    Faddah, Dina A.
    Kieckhaefer, Julia E.
    Olive, Michelle
    Erdos, Michael R.
    Nabel, Elizabeth G.
    Collins, Francis S.
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2011, 121 (07) : 2833 - 2844
  • [7] Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence
    Caron, M.
    Auclair, M.
    Donadille, B.
    Bereziat, V.
    Guerci, B.
    Laville, M.
    Narbonne, H.
    Bodemer, C.
    Lascols, O.
    Capeau, J.
    Vigouroux, C.
    [J]. CELL DEATH AND DIFFERENTIATION, 2007, 14 (10) : 1759 - 1767
  • [8] Autophagic degradation of farnesylated prelamin A as a therapeutic approach to lamin-linked progeria
    Cenni, V.
    Capanni, C.
    Columbaro, M.
    Ortolani, M.
    D'Apice, M. R.
    Novelli, G.
    Fini, M.
    Marmiroli, S.
    Scarano, E.
    Maraldi, N. M.
    Squarzoni, S.
    Prencipe, S.
    Lattanzi, G.
    [J]. EUROPEAN JOURNAL OF HISTOCHEMISTRY, 2011, 55 (04): : 200 - 205
  • [9] Oxidative stress implication in a new phenotype of amyotrophic quadricipital syndrome with cardiac involvement due to lamin A/C mutation
    Charniot, J. C.
    Bonnefont-Rousselot, D.
    Marchand, C.
    Zerhouni, K.
    Vignat, N.
    Peynet, J.
    Plotkine, M.
    Legrand, A.
    Artigou, J. Y.
    [J]. FREE RADICAL RESEARCH, 2007, 41 (04) : 424 - 431
  • [10] Erythrocyte Senescence in a Model of Rat Displaying Hutchinson-Gilford Progeria Syndrome
    Chaudhary, Manoj Kumar
    Rizvi, Syed Ibrahim
    [J]. ANALYTICAL CELLULAR PATHOLOGY, 2018, 2018