About this Research Topic
Mitochondria are dynamic organelles that play a crucial role in energy production in the form of adenosine triphosphate (ATP). Beyond their primary role in bioenergetics, mitochondria are involved in regulating cellular metabolism, apoptosis, and calcium homeostasis. The maintenance of healthy and functional mitochondria – in terms of optimal numbers and morphology are essential to cell survival. Mitochondrial dysfunction, characterized by impaired ATP production and elevated production of reactive oxygen species (ROS), leads to increased oxidative stress, a contributing factor in the pathogenesis of numerous disorders.
Mitochondrial dysfunction plays a pivotal role in both neurological and cardiovascular diseases through several mechanisms. In neurological disorders, impaired mitochondrial function can lead to neuronal loss and synaptic dysfunction, contributing to the progression of diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), Friedreich's ataxia (FRDA), and amyotrophic lateral sclerosis (ALS). These conditions are often marked by energy deficits, increased deleterious ROS, and disrupted calcium homeostasis, which collectively result in neurodegeneration. In cardiovascular diseases, including atherosclerosis, hypertension, cardiomyopathy, myocardial ischemia and reperfusion injury, heart failure, and cardiomyopathy, similar etiological factors lead to mitochondrial dysfunction causing cardiovascular damage. The heart’s and brain's high demand for energy makes them particularly susceptible and vulnerable to mitochondrial impairments, which can lead to compromised function and disease progression.
As millions of patients globally continue to suffer from neurological and cardiovascular diseases, further understanding the pathophysiology of these disorders remains crucial. For this reason, the goal of this Research Topic is twofold, firstly, to bring together cutting-edge research, both basic and clinical, focused on understanding the mechanistic underpinnings that belie mitochondrial dysfunction in neurodegenerative and cardiovascular diseases; and secondly, to identify novel therapeutic approaches targeting mitochondrial dysfunction in these disorders, with the overall aim of abating or preventing disease progression.
Submissions of Original Research articles, Reviews, and Mini-Reviews on the following themes are of particular interest, but other relevant papers are welcome.
• Mechanisms of mitochondrial dysfunction in neurodegenerative and cardiovascular diseases
• Innovative strategies to enhance mitochondrial biogenesis and function
• The role of mitochondrial dynamics and quality control and mitophagy in disease progression
• Therapeutic approaches targeting mitochondria, including excess ROS production, calcium homeostasis, mtDNA, etc.
• Nutritional, including caloric restriction, and pharmacological interventions to support mitochondrial health
• Biomarkers for mitochondrial dysfunction in neurological and cardiovascular diseases
• Preclinical and clinical studies on mitochondrial-targeted therapies
• Mitochondria-targeted drug delivery systems
• The impact of lifestyle and environmental factors on mitochondrial function
Mitochondrial dysfunction plays a pivotal role in both neurological and cardiovascular diseases through several mechanisms. In neurological disorders, impaired mitochondrial function can lead to neuronal loss and synaptic dysfunction, contributing to the progression of diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), Friedreich's ataxia (FRDA), and amyotrophic lateral sclerosis (ALS). These conditions are often marked by energy deficits, increased deleterious ROS, and disrupted calcium homeostasis, which collectively result in neurodegeneration. In cardiovascular diseases, including atherosclerosis, hypertension, cardiomyopathy, myocardial ischemia and reperfusion injury, heart failure, and cardiomyopathy, similar etiological factors lead to mitochondrial dysfunction causing cardiovascular damage. The heart’s and brain's high demand for energy makes them particularly susceptible and vulnerable to mitochondrial impairments, which can lead to compromised function and disease progression.
As millions of patients globally continue to suffer from neurological and cardiovascular diseases, further understanding the pathophysiology of these disorders remains crucial. For this reason, the goal of this Research Topic is twofold, firstly, to bring together cutting-edge research, both basic and clinical, focused on understanding the mechanistic underpinnings that belie mitochondrial dysfunction in neurodegenerative and cardiovascular diseases; and secondly, to identify novel therapeutic approaches targeting mitochondrial dysfunction in these disorders, with the overall aim of abating or preventing disease progression.
Submissions of Original Research articles, Reviews, and Mini-Reviews on the following themes are of particular interest, but other relevant papers are welcome.
• Mechanisms of mitochondrial dysfunction in neurodegenerative and cardiovascular diseases
• Innovative strategies to enhance mitochondrial biogenesis and function
• The role of mitochondrial dynamics and quality control and mitophagy in disease progression
• Therapeutic approaches targeting mitochondria, including excess ROS production, calcium homeostasis, mtDNA, etc.
• Nutritional, including caloric restriction, and pharmacological interventions to support mitochondrial health
• Biomarkers for mitochondrial dysfunction in neurological and cardiovascular diseases
• Preclinical and clinical studies on mitochondrial-targeted therapies
• Mitochondria-targeted drug delivery systems
• The impact of lifestyle and environmental factors on mitochondrial function
Keywords: Cardiovascular Diseases, Alzheimer's Disease (AD), Ca2+ Homeostasis, Oxidative Stress, Drug target, Mitochondrial dysfunction, Parkinson's disease (PD), Huntington's disease (HD), Friedreich's ataxia (FRDA), amyotrophic lateral sclerosis (ALS)
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
