Blood biomarkers for assessment of mitochondrial dysfunction: An expert review

Hubens, Wouter; Vallbona-Garcia, Antoni; Coo, I.F.M. de; Tienen, F.H.J. van; Webers, Casper; Smeets, Hubert J.M.; Gorgels, T. G. M. F.

doi:10.1016/j.mito.2021.10.008

Cited by 29 publications

(28 citation statements)

References 206 publications

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“…Thus, we speculate that the underlying pathology might account for the upregulation of carnitine and acyl carnitines in these patients, suggesting their putative role as future diagnostic markers. However, elevation of lactate in mitochondrial dysfunction is usually condition dependent [55], accounting for the reduced lactate levels in our cases as compared to controls.…”

Section: Discussionmentioning

confidence: 86%

Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

Ghosh

Singh

Govil

et al. 2022

Preprint

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Background Minimal change disease (MCD), a glomerular disease subtype is characterised by no visible change in the glomerulus upon light microscopy except for the urinary excretion of excess proteins. The symptoms of minimal change disease and renal amyloidosis are mostly overlapping and thereby misdiagnosed. However, the possible linkage between these two disease types has not been documented. We hypothesised that amyloid formation could be one of the players promoting the pathology associated with minimal change disease, resulting in perturbations of the downstream cellular pathways. Methods One hundred glomerular diseased patients were identified in a two-year study, based on symptoms and biochemical markers. Histopathological analysis showed predominance of minimal change disease in twenty patients. Further, gold standard Congo red staining was performed in these patients to detect amyloid deposition followed by tracking its downstream effects on cellular pathways using mass-spectrometry-based untargeted approach. Results Congo red staining showed presence of amyloid deposits in eleven minimal change diseased patients. Further, plasma metabolomic fingerprinting revealed a total of fifteen biologically important metabolites altered in minimal change diseased patients having renal amyloidosis as compared to controls. Different classes of lipids, carnitines and amino acids were found to be dysregulated in these patients. Conclusion In the present study we have shown the onset of renal amyloidosis and associated pathogenesis in minimal change diseased patients. Additionally, we have identified novel altered metabolic signatures in these patients as compared to controls. This is the first study in context to the Indian population, depicting the potential of metabolomic fingerprinting to identify novel markers for early diagnosis of amyloid formation in minimal change disease, a glomerular disease type.

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Section: Discussionmentioning

confidence: 86%

Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

Ghosh

Singh

Govil

et al. 2022

Preprint

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“…Mitochondrial fission and fusion impairments have been related to the development of cardiovascular diseases [ 28 ]. Novel mitochondrial biomarkers have been proposed to identify patients that can benefit from therapies specifically targeting mitochondria [ 29 ].…”

Section: Mechanism Of Mitochondrial Dysfunction and Molecular Implica...mentioning

confidence: 99%

Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?

Ciccarelli

Conte

Cimmino

et al. 2023

IJMS

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Atherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, a significant residual risk is still relevant, and is related to unmet therapeutic targets. Endothelial dysfunction and lipid infiltration are the primary causes of atherosclerotic plaque progression. In this contest, mitochondrial dysfunction can affect arterial wall cells, in particular macrophages, smooth muscle cells, lymphocytes, and endothelial cells, causing an increase in reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and intracellular lipid deposition. The detection and characterization of mitochondrial DNA (mtDNA) is crucial for assessing mitochondrial defects and should be considered the goal for new future therapeutic interventions. In this review, we will focus on a new idea, based on the analysis of data from many research groups, namely the link between mitochondrial impairment and endothelial dysfunction and, in particular, its effect on atherosclerosis and aging. Therefore, we discuss known and novel mitochondria-targeting therapies in the contest of atherosclerosis.

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“…If the reduced perfusion leads to a shortage in the oxygen supply to the brain, the mitochondria in neurons suffer. Sufficient evidence already exists in various neurodegenerative diseases pointing to alterations in mitochondrial function [67][68][69][70][71][72][73][74]. In short, would it make sense that a shortage of blood would affect the mitochondria and ultimately lead to neuronal death?…”

Section: Pills To Reduce Glycemia Impact On Neuronal Survivalmentioning

confidence: 99%

Can chronic therapeutic drug use by the elderly affect Alzheimer’s disease risk and rate of progression?

Franco

Serrano-Marín

2023

Explor Neuroprot Ther

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There is no approved drug capable of halting the progression of the most prevalent neurodegenerative disorders, namely Alzheimer’s disease (AD) and Parkinson’s disease (PD). Current therapeutic strategies focus mainly on the inhibition of the formation of protein aggregates and their deposition in the central nervous system. However, after almost a hundred years, proper management of the disease is still lacking. The fact of not finding effective management tools in the various clinical trials already carried out suggests that new hypotheses and strategies should be explored. Although vast resources have been allocated to the investigation of protein aggregates and the pathophysiology is now better understood, clues to the actual etiology are lacking. It is well known that brain homeostasis is of paramount importance for the survival of neurons. Drugs that target the periphery are often not subject to evaluation for their potential effect on the central nervous system. While acute treatments may be irrelevant, pills used for chronic conditions can be detrimental to neurons, especially in terms of progressive damage leading to a long-term decline in neuronal survival. Due to the lack of advances in the search for a curative treatment for neurodegenerative diseases, and the lack of new hypotheses about their etiology, a novel hypothesis is here proposed. It consists of assuming that the effects of the drugs most commonly used by the elderly, such as antihypertensive, hypoglycemic, and hypocholesterolemic, could have a negative impact on neuronal survival.

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Blood biomarkers for assessment of mitochondrial dysfunction: An expert review

Cited by 29 publications

References 206 publications

Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?

Can chronic therapeutic drug use by the elderly affect Alzheimer’s disease risk and rate of progression?

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