KLF4 in Parkinson’s Disease: Decoding the Molecular Puzzle of Neuroinflammation, Oxidative Stress, and Emerging Therapies

Abstract

Parkinson’s disease (PD) is the most prevalent neurodegenerative movement condition. Tremors, stiffness, bradykinesia/akinesia, and postural instability are its primary motor symptoms; nevertheless, the clinical features also include non-motor and additional motor symptoms. Krüppel-like factor 4 (KLF4), a zinc finger transcription factor, is present in several human tissues and performs a range of cell-dependent regulatory actions. Various neurological diseases, such as PD, Alzheimer’s disease (AD), and Huntington’s disease (HD), have been linked to KLF4, which regulates some neurophysiological and neuropathological processes in the brain. Recent data indicate that KLF4 plays a crucial regulatory role in the neurophysiological and neuropathological processes underlying PD, suggesting that it might be a viable therapeutic target for neurodegenerative diseases. This review focuses on the potential molecular mechanism underlying KLF4-mediated neuroinflammation, oxidative stress, mitochondrial dysfunction, and apoptosis. KLF4-mediated pathways are clarified by the information gathered here, and targeting them appears to be a viable therapeutic strategy for treating PD. Nevertheless, there is insufficient information on this subject, and more investigations are needed to fully understand the translational significance of the KLF4-oriented therapeutic strategy in PD.

Keywords

Parkinson’s disease / Krüppel-like factor 4 / Neuroinflammation / Oxidative stress / Mitochondrial dysfunction / Apoptosis / Programmed cell death

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