How does mitochondrial biogenesis dysfunction effects on cellular homeostasis and physiology?
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Mitochondrial biogenesis dysfunction significantly impacts cellular homeostasis and physiology. Impaired protein import into mitochondria due to various stressors leads to the accumulation of precursor proteins in the cytosol, activating stress response pathways. This disruption triggers a network of processes involving transcription, translation, and protein clearance to restore cellular protein homeostasis. Additionally, mitochondrial dysfunction, particularly protein import defects, results in the formation of aberrant protein deposits in the cytosol, leading to the aggregation of disease-related proteins like α-synuclein and amyloid β, causing a cytosolic protein homeostasis imbalance. Mitochondrial dysfunction also affects cellular functions like oxidative phosphorylation, calcium homeostasis, and biomolecule synthesis, ultimately impacting overall cellular health.
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43 Citations | Mitochondrial biogenesis dysfunction disrupts cellular proteostasis, leading to impaired mitochondrial function, increased reactive oxygen species, and potential cell death, impacting cellular homeostasis and physiology. |
34 Citations | Mitochondrial biogenesis dysfunction disrupts cellular homeostasis, leading to metabolic diseases and aging. Exercise helps prevent and delay such dysfunction by enhancing mitochondrial metabolism and quality control mechanisms. |
26 Citations | Mitochondrial protein import failures lead to cytosolic aggregation, disrupting protein homeostasis. This triggers further aggregation of mitochondrial and disease-related proteins, impacting cellular homeostasis and potentially contributing to neurodegenerative diseases. |
| Mitochondrial biogenesis dysfunction disrupts cellular homeostasis by impairing functions like oxidative phosphorylation, calcium regulation, and biomolecule synthesis, impacting overall cellular physiology and contributing to neurodegenerative conditions. | |
24 Citations | Mitochondrial biogenesis dysfunction disrupts cellular protein homeostasis, triggering stress responses involving transcription, translation, and protein clearance mechanisms to restore cellular equilibrium. |
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How does mitochondrial function impact cellular metabolism and energy production?4 answersMitochondria play a crucial role in cellular metabolism and energy production. These organelles are known as the cellular powerhouses due to their involvement in oxidative phosphorylation (OXPHOS), which is the primary process for energy generation. Mitochondria communicate with the nucleus and other organelles to maintain cellular homeostasis, adapt to stress, and influence cell fate decisions. Dysregulation of mitochondrial function is linked to various prevalent diseases like type 2 diabetes, cardiovascular disease, cancer, and neurodegenerative disorders. Additionally, mitochondria are essential for reactive oxygen species production, fatty acid metabolism, and epigenetic remodeling, impacting stem cell fate decisions and tissue regeneration. The balance between glycolysis and OXPHOS is crucial for ATP generation, with mitochondrial dysfunction contributing significantly to disease pathogenesis.
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What role does mitochondrial biogenesis play in OA?5 answersMitochondrial biogenesis plays an important role in the pathogenesis of osteoarthritis (OA). It has been shown that mitochondria are significant energy metabolic centers in chondrocytes, and dysfunction of mitochondria is considered an essential mechanism in the development of OA. Mitochondrial biogenesis is a key process that maintains the normal quantity and function of mitochondria, and the central regulator of this process is peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α). There is a regulatory network of mitochondrial biogenesis involving various signaling molecules, such as adenosine monophosphate-activated protein kinase, sirtuin1/3, and cyclic adenosine monophosphate response element-binding protein. Furthermore, substances like puerarin and omentin-1 have shown potential in activating damaged mitochondrial biogenesis in OA chondrocytes, suggesting their potential use in OA treatment. The mitochondrial genetic background also influences the prevalence, severity, incidence, and progression of OA, possibly through the regulation of energy production, reactive oxygen species generation, apoptosis, and inflammation. Therefore, mitochondrial biogenesis is a promising therapeutic target for OA.
Does mitochondrial dysfunction lead to chondrocyte dysfunction?5 answersMitochondrial dysfunction has been shown to contribute to chondrocyte dysfunction in osteoarthritis (OA). Studies have demonstrated that mitochondrial dysfunction in chondrocytes is associated with OA and can lead to increased chondrocyte apoptosis, decreased type II collagen secretion, and cartilage degeneration. Furthermore, mitochondrial dysfunction-induced activation of the catabolic response in chondrocytes has been observed, resulting in the expression of catabolic genes involved in OA pathogenesis. Mechanical stress, a major risk factor for OA, has also been shown to affect mitochondrial function in chondrocytes, with moderate stress maintaining mitochondrial function and reducing apoptosis, while excessive stress leading to mitochondrial dysfunction and apoptosis. These findings highlight the importance of mitochondrial homeostasis in chondrocyte function and suggest that targeting mitochondrial dysfunction may be a potential therapeutic strategy for OA management.
Does mitochondrial dysfunction contribute to the development of diet-induced insulin resistance?2 answersMitochondrial dysfunction has been shown to contribute to the development of diet-induced insulin resistance. Studies have demonstrated that impaired mitochondrial function, including reduced ATP production, citrate synthase activity, and mitochondrial respiration, occurs coincidently with insulin resistance in skeletal muscle. Additionally, mitochondrial dysfunction has been associated with insulin resistance in adipose tissue, liver, and skeletal muscle, which are all involved in food metabolism. Furthermore, improving mitochondrial function has been found to attenuate insulin resistance, suggesting that targeting mitochondrial dysfunction may have therapeutic potential for treating insulin resistance. The toxic effects of drugs and pollutants on mitochondria have also been reported to potentially compromise insulin sensitivity, highlighting the importance of understanding drug-induced mitochondrial toxicity in the development of insulin resistance. In summary, the evidence suggests that mitochondrial dysfunction plays a significant role in the development of diet-induced insulin resistance.