Mitochondrial dysfunction

Mitochondrial dysfunction refers to any condition or impairment that disrupts the normal functioning of mitochondria, which are organelles found in the cytoplasm of eukaryotic cells. Mitochondria are often referred to as the “powerhouses” of the cell because they play a critical role in generating energy in the form of adenosine triphosphate (ATP) through a process called oxidative phosphorylation.

Mitochondrial dysfunction can manifest in various ways and can be caused by a range of factors, including genetic mutations, environmental toxins, metabolic disorders, and aging. Some common consequences of mitochondrial dysfunction include:

Reduced ATP Production: Since ATP is the primary energy currency of the cell, mitochondrial dysfunction can lead to decreased energy levels, which may impair cellular processes and overall bodily function.

Increased Reactive Oxygen Species (ROS) Production: Mitochondria produce ROS as a byproduct of ATP synthesis. However, excessive ROS production due to mitochondrial dysfunction can lead to oxidative stress, causing damage to cellular components such as DNA, proteins, and lipids.

Impaired Calcium Homeostasis: Mitochondria play a role in regulating intracellular calcium levels. Dysfunction in this process can disrupt cellular signaling and lead to various pathological conditions.

Apoptosis Dysregulation: Mitochondria are involved in the regulation of apoptosis, or programmed cell death. Dysfunction in this process can either inhibit apoptosis, leading to cell survival when it should die, or promote excessive cell death.

Metabolic Disorders: Mitochondria are involved in various metabolic pathways, including the metabolism of carbohydrates, fats, and amino acids. Dysfunction in mitochondrial metabolism can lead to metabolic disorders such as diabetes, obesity, and fatty liver disease.

Neurodegenerative Diseases: Mitochondrial dysfunction has been implicated in the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis (ALS). In these conditions, mitochondrial dysfunction may contribute to neuronal cell death and the progression of the disease.

Treatment of mitochondrial dysfunction can vary depending on the underlying cause and specific symptoms but may include lifestyle modifications, dietary interventions, supplements, and medications aimed at supporting mitochondrial function and reducing oxidative stress. In some cases, gene therapy or mitochondrial replacement therapy may be considered for inherited mitochondrial disorders.

Glucagon-like peptide-1 receptor (GLP1R) agonist has gained interest as a potential treatment for Parkinson's disease (PD). However, the exact mechanisms responsible for the therapeutic effects of GLP-1R-related agonists are not yet fully understood.

Wang et al. explores the effects of early treatment with PT320, a sustained release formulation of the GLP-1R agonist Exenatide, on mitochondrial functions and morphology in a progressive PD mouse model, the MitoPark (MP) mouse.

The findings demonstrate that administration of a clinically translatable dose of PT320 ameliorates the reduction in tyrosine hydroxylase expression, lowers reactive oxygen species (ROS) levels, and inhibits mitochondrial cytochrome c release during nigrostriatal dopaminergic denervation in MP mice. PT320 treatment significantly preserved mitochondrial function and morphology but did not influence the reduction in mitochondria numbers during PD progression in MP mice. Genetic analysis indicated that the cytoprotective effect of PT320 is attributed to a reduction in the expression of mitochondrial fission protein 1 (Fis1) and an increase in the expression of optic atrophy type 1 (Opa1), which is known to play a role in maintaining mitochondrial homeostasis and decreasing cytochrome c release through remodeling of the cristae.

The findings suggest that the early administration of PT320 shows potential as a neuroprotective treatment for PD, as it can preserve mitochondrial function. Through enhancing mitochondrial health by regulating Opa1 and Fis1, PT320 presents a new neuroprotective therapy in PD ¹⁾

Mitochondrial dysfunction contributes to the development of secondary brain injury (SBI) following intracerebral hemorrhage (ICH) and represents a promising therapeutic target. Celastrol, the primary active component of Tripterygium wilfordii, is a natural product that exhibits mitochondrial and neuronal protection in various cell types. This study aims to investigate the neuroprotective effects of celastrol against ICH-induced SBI and explore its underlying mechanisms. Celastrol improves neurobehavioral and cognitive abilities in mice with autologous blood-induced ICH, reduces neuronal death in vivo and in vitro, and promotes mitochondrial function recovery in neurons. Single-cell nuclear sequencing reveals that the cyclic adenosine monophosphate (cAMP)/cAMP-activated exchange protein-1 (EPAC-1) signaling pathways are impacted by celastrol. Celastrol binds to cNMP (a domain of EPAC-1) to inhibit its interaction with voltage-dependent anion-selective channel protein 1 (VDAC1) and blocks the opening of mitochondrial permeability transition pores. After neuron-specific knockout of EPAC1, the neuroprotective effects of celastrol are diminished. In summary, this study demonstrates that celastrol, through its interaction with EPAC-1, ameliorates mitochondrial dysfunction in neurons, thus potentially improving SBI induced by ICH. These findings suggest that targeting EPAC-1 with celastrol can be a promising therapeutic approach for treating ICH-induced SBI ²⁾

Peripheral nerve injury (PNI) can lead to mitochondrial dysfunction and energy depletion within the affected microenvironment. The objective was to investigate the potential of transplanting mitochondria to reshape the neural regeneration microenvironment. High-purity functional mitochondria with an intact structure were extracted from Human umbilical cord-derived mesenchymal stem cells (hUCMSCs) using the Dounce homogenization combined with ultracentrifugation. Results showed that when hUCMSC-derived mitochondria (hUCMSC-Mitos) were co-cultured with Schwann cells (SCs), they promoted the proliferation, migration, and respiratory capacity of SCs. Acellular nerve allografts (ANAs) have shown promise in nerve regeneration, however, their therapeutic effect is not satisfactory enough. The incorporation of hUCMSC-Mitos within ANAs (referred to as Mito-ANAs) has the potential to remodel the regenerative microenvironment. This approach demonstrated satisfactory outcomes in terms of tissue regeneration and functional recovery. Particularly, we propose for the first time the use of metabolomics and bioenergetic profiling to analyze the energy metabolism microenvironment after PNI. This remodeling occurs through the enhancement of the tricarboxylic acid (TCA) cycle and the regulation of associated metabolites, resulting in increased energy synthesis. Overall, the hUCMSC-Mito-loaded ANAs exhibited high functionality to promote nerve regeneration, providing a novel regenerative strategy based on improving energy metabolism for neural repair ³⁾

Mitochondrial dysfunction in traumatic brain injury

Mitochondrial dysregulation is a pivotal hallmark of aging-related disorders. Although there is a considerable understanding of the molecular counteracting responses toward damaged mitochondria, the molecular underpinnings connecting the abnormal aggregation of mitochondrial precursor protein fragments and abrogation of mitochondrial import machinery are far from clear. Proteasomal-dependent degradation was unveiled as a pivotal fine-tuner of TOM machinery-dependent mitochondrial import ⁴⁾.

Mitochondrial dysfunction occurs when the mitochondria do not work as well as they should due to another disease or condition.

Mitochondrial dysfunction is characterised by an increased Lactate to Pyruvate Ratio (LP ratio) signifying a shift in cytoplasmatic redox state at normal or elevated Partial pressure of brain tissue oxygen . The condition is biochemically characterised by a marked increase in cerebral lactate with a normal or elevated pyruvate level. The metabolic pattern is different from cerebral ischemia, which is characterised by simultaneous decreases in intracerebral pyruvate and PbtO2 . The study supports the hypothesis that cerebral ischemia and mitochondrial dysfunction may be identified and separated at the bedside by utilising intracerebral microdialysis ⁵⁾.

In a study of Engquist et al. from Uppsala, CBF was assessed by bedside xenon CT at days 0-3, 4-7, and 8-12, and the cerebral metabolic state by cerebral microdialysis (CMD), analyzing glucose, lactate, pyruvate, and glutamate hourly. At clinical suspicion of DCI, HHH therapy was instituted for 5 days. Cerebral blood flow measurements and CMD data at baseline and during HHH therapy were required for study inclusion. Non-DCI patients with measurements in corresponding time windows were included as a reference group.

In DCI patients receiving HHH therapy (n = 12), global cortical CBF increased from 30.4 ml/100 g/min (IQR 25.1-33.8 ml/100 g/min) to 38.4 ml/100 g/min (IQR 34.2-46.1 ml/100 g/min; p = 0.006). The energy metabolic CMD parameters stayed statistically unchanged with a Lactate to Pyruvate Ratio of 26.9 (IQR 22.9-48.5) at baseline and 31.6 (IQR 22.4-35.7) during HHH. Categorized by energy metabolic patterns during HHH, no patient had severe ischemia, 8 showed derangement corresponding to mitochondrial dysfunction, and 4 were normal. The reference group of non-DCI patients (n = 11) had higher CBF and lower L/P ratios at baseline with no change over time, and the metabolic pattern was normal in all these patients.

Global and regional CBF improved and the cerebral energy metabolic CMD parameters stayed statistically unchanged during HHH therapy in DCI patients. None of the patients developed metabolic signs of severe ischemia, but a disturbed energy metabolic pattern was a common occurrence, possibly explained by mitochondrial dysfunction despite improved microcirculation ⁶⁾

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Wang V, Tseng KY, Kuo TT, Huang EY, Lan KL, Chen ZR, Ma KH, Greig NH, Jung J, Choi HI, Olson L, Hoffer BJ, Chen YH. Attenuating mitochondrial dysfunction and morphological disruption with PT320 delays dopamine degeneration in MitoPark mice. J Biomed Sci. 2024 Apr 17;31(1):38. doi: 10.1186/s12929-024-01025-6. PMID: 38627765.

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Li X Sr, Liu W, Jiang G, Lian J, Zhong Y, Zhou J, Li H, Xu X, Liu Y, Cao C, Tao J, Cheng J, Zhang JH, Chen G. Celastrol Ameliorates Neuronal Mitochondrial Dysfunction Induced by Intracerebral Hemorrhage via Targeting cAMP-Activated Exchange Protein-1. Adv Sci (Weinh). 2024 Mar 14:e2307556. doi: 10.1002/advs.202307556. Epub ahead of print. PMID: 38482725.

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Mitochondrial dysfunction

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