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Research Article Open access CC BY 4.0

Mitochondria and Nuclear Interaction: Cellular Insights and Implications in Neurodegenerative Diseases

Kiran Kumar H.B, Mahalakshmi B.R., Priya M.D., Santhosh D.B, BK Manjunatha, Sajeeda Niketh, Valarmathy K

Asian Journal of Biology · pp. 59–79 · Published 30 Jun 2025

10.9734/ajob/2025/v21i7529

Abstract

Mitochondria are organelles known as the "powerhouses" of the cell that produce energy. They are centers that have roles in producing heat, storing calcium, and controlling cell division and death. To this end each of the several compartments or areas that make up mitochondria has a specific function. Several researchers report unusual cytological features of mitochondria, such as proximity to the nucleus and different shapes in both normal and aberrant conditions. Aided by several proteins and processes, several proteins are shuttled from the mitochondria to the nucleus and vice versa at the cellular level. Mitochondria and nucleus are essential for cellular important functions such as energy production, metabolism, and cell proliferation. Additionally, the transport shapes, and functions of mitochondria are crucial for a number of cellular processes specifically neuronal functions. The cyto-architecture and distinct physiological adaptations of cells in both healthy and diseased conditions are included in this review, which provides an update in this field of mitochondrial biology. We specifically concentrate on the function of mitochondria and mitochondria-nuclear transport in brain since neurons play special roles beyond energy production. These functions include preserving calcium homeostasis, controlling the metabolism of fats and carbohydrates, and generating reactive oxygen species (ROS), all of which are essential for the proper operation of the brain. A number of neurodegenerative illnesses exhibit altered nuclear proteins, aberrant mitochondrial morphology, metabolic dysfunction and interaction dysfunctions. Lastly, mitochondria have emerged as a potentially useful therapeutic target in several human mitochondrial diseases. The present review is an update to bridge several knowledge gaps that exist regarding the mitochondrial dysfunction in neurodegeneration.

Endosymbiotic alphaproteobacterium Oxidative phosphorylation (OXPHOS) mitochondrial DNA (mtDNA) kinesin

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