Mitochondrial quality control (MQC) is a critical process in eukaryotic cells that maintains mitochondrial function and integrity. MQC involves three main mechanisms: mitochondrial biogenesis, mitochondrial dynamics (fusion and fission), and mitophagy. These processes are essential for regulating energy metabolism, cell proliferation, differentiation, immune responses, and redox balance. MQC helps eliminate damaged mitochondria, maintain mitochondrial function, and prevent the accumulation of dysfunctional mitochondria, which can lead to cellular and organ dysfunction. Mitochondrial biogenesis is a tightly regulated process that involves the coordinated expression of nuclear and mitochondrial genes to increase mitochondrial size and number. Key regulators include PGC-1α, which activates mitochondrial biogenesis by promoting the transcription of mitochondrial proteins and mtDNA replication. PGC-1α also interacts with PPARs and ERRs to regulate mitochondrial function and energy metabolism. Other regulators include AMPK, which senses energy levels and activates PGC-1α to promote mitochondrial biogenesis. CaMK and Sirt1 also play roles in regulating mitochondrial biogenesis through various signaling pathways. Mitochondrial dynamics involve the balance between fusion and fission, which is crucial for maintaining mitochondrial morphology and function. Mitofusins (MFNs) and optic atrophy 1 (OPA1) are key regulators of mitochondrial fusion, while DRP1 is a key regulator of mitochondrial fission. These processes are regulated by post-translational modifications, such as phosphorylation, deacetylation, and ubiquitination, which modulate the activity and function of these proteins. Mitophagy is a selective process that removes damaged mitochondria through autophagy. It is mediated by the PINK1/Parkin pathway, which marks damaged mitochondria for degradation. Other mitophagy receptors, such as BNIP3, BNIP3L (Nix), and FUNDC1, also play roles in targeting damaged mitochondria for degradation. These processes are essential for maintaining mitochondrial homeostasis and preventing the accumulation of dysfunctional mitochondria, which can lead to various diseases, including cancer, cardiovascular disease, metabolic disorders, and neurodegenerative diseases. Understanding the molecular mechanisms of MQC is crucial for developing therapeutic strategies to treat mitochondrial dysfunction and related diseases. Targeting MQC pathways can enhance mitochondrial function and improve cellular and organismal health.Mitochondrial quality control (MQC) is a critical process in eukaryotic cells that maintains mitochondrial function and integrity. MQC involves three main mechanisms: mitochondrial biogenesis, mitochondrial dynamics (fusion and fission), and mitophagy. These processes are essential for regulating energy metabolism, cell proliferation, differentiation, immune responses, and redox balance. MQC helps eliminate damaged mitochondria, maintain mitochondrial function, and prevent the accumulation of dysfunctional mitochondria, which can lead to cellular and organ dysfunction. Mitochondrial biogenesis is a tightly regulated process that involves the coordinated expression of nuclear and mitochondrial genes to increase mitochondrial size and number. Key regulators include PGC-1α, which activates mitochondrial biogenesis by promoting the transcription of mitochondrial proteins and mtDNA replication. PGC-1α also interacts with PPARs and ERRs to regulate mitochondrial function and energy metabolism. Other regulators include AMPK, which senses energy levels and activates PGC-1α to promote mitochondrial biogenesis. CaMK and Sirt1 also play roles in regulating mitochondrial biogenesis through various signaling pathways. Mitochondrial dynamics involve the balance between fusion and fission, which is crucial for maintaining mitochondrial morphology and function. Mitofusins (MFNs) and optic atrophy 1 (OPA1) are key regulators of mitochondrial fusion, while DRP1 is a key regulator of mitochondrial fission. These processes are regulated by post-translational modifications, such as phosphorylation, deacetylation, and ubiquitination, which modulate the activity and function of these proteins. Mitophagy is a selective process that removes damaged mitochondria through autophagy. It is mediated by the PINK1/Parkin pathway, which marks damaged mitochondria for degradation. Other mitophagy receptors, such as BNIP3, BNIP3L (Nix), and FUNDC1, also play roles in targeting damaged mitochondria for degradation. These processes are essential for maintaining mitochondrial homeostasis and preventing the accumulation of dysfunctional mitochondria, which can lead to various diseases, including cancer, cardiovascular disease, metabolic disorders, and neurodegenerative diseases. Understanding the molecular mechanisms of MQC is crucial for developing therapeutic strategies to treat mitochondrial dysfunction and related diseases. Targeting MQC pathways can enhance mitochondrial function and improve cellular and organismal health.