Mitochondria play a central role in cellular metabolism, acting as the primary source of ATP through oxidative phosphorylation. They are highly dynamic organelles that undergo fusion, fission, transport, and mitophagy, processes crucial for maintaining a healthy mitochondrial population. The review discusses how these dynamic processes are influenced by cellular signaling events and how they affect metabolism. **Metabolic Control of Mitochondrial Fusion:** Mitochondrial fusion is mediated by GTPases such as mitofusin 1 (Mfn1), Mfn2, and optic atrophy 1 (Opa1). Fusion is a two-step process involving outer and inner membrane fusion. The balance between fusion and fission controls mitochondrial morphology. Genetic deletion of fusion genes leads to mitochondrial fragmentation and impaired respiratory chain activity. Metabolic conditions, such as increased OXPHOS activity, promote mitochondrial fusion by stimulating the proteolytic processing of Opa1, which activates its fusion activity. **Metabolic Control of Mitochondrial Fission:** Fission is mediated by dynamin-related protein 1 (Drp1), which is recruited to the mitochondrial surface via receptor proteins. Phosphorylation of Drp1 at specific sites, such as serine 616 (S616) and S637, regulates its activity. PKA phosphorylation at S637 inhibits Drp1 activity, promoting mitochondrial elongation. In contrast, AMPK activation during energy stress phosphorylates Drp1 at S616, enhancing fission. Cold exposure and hypoxia also activate fission through distinct pathways involving calcineurin and PGAM5, respectively. **Metabolic Control of Mitochondrial Transport:** Mitochondrial transport is primarily mediated by microtubule-dependent motors like kinesin. Glucose levels in synapses can influence mitochondrial transport, affecting energy consumption and signaling processes. **Metabolic Control of Mitophagy:** Mitophagy is a process that removes dysfunctional mitochondria through autophagy. The Pink1/Parkin pathway is best studied, where Pink1 accumulates on depolarized mitochondria and recruits Parkin, an E3 ligase, to ubiquitinate and target mitochondria for degradation. AMPK activation during energy stress also promotes mitophagy by activating ULK1 and ULK2, which promote autophagy. Hypoxic conditions trigger mitophagy through the dephosphorylation of FUNDC1 by PGAM5, promoting autophagic membrane formation. The review highlights the complex interplay between mitochondrial dynamics and metabolism, emphasizing the importance of understanding these processes for therapeutic interventions in diseases related to mitochondrial dysfunction.Mitochondria play a central role in cellular metabolism, acting as the primary source of ATP through oxidative phosphorylation. They are highly dynamic organelles that undergo fusion, fission, transport, and mitophagy, processes crucial for maintaining a healthy mitochondrial population. The review discusses how these dynamic processes are influenced by cellular signaling events and how they affect metabolism. **Metabolic Control of Mitochondrial Fusion:** Mitochondrial fusion is mediated by GTPases such as mitofusin 1 (Mfn1), Mfn2, and optic atrophy 1 (Opa1). Fusion is a two-step process involving outer and inner membrane fusion. The balance between fusion and fission controls mitochondrial morphology. Genetic deletion of fusion genes leads to mitochondrial fragmentation and impaired respiratory chain activity. Metabolic conditions, such as increased OXPHOS activity, promote mitochondrial fusion by stimulating the proteolytic processing of Opa1, which activates its fusion activity. **Metabolic Control of Mitochondrial Fission:** Fission is mediated by dynamin-related protein 1 (Drp1), which is recruited to the mitochondrial surface via receptor proteins. Phosphorylation of Drp1 at specific sites, such as serine 616 (S616) and S637, regulates its activity. PKA phosphorylation at S637 inhibits Drp1 activity, promoting mitochondrial elongation. In contrast, AMPK activation during energy stress phosphorylates Drp1 at S616, enhancing fission. Cold exposure and hypoxia also activate fission through distinct pathways involving calcineurin and PGAM5, respectively. **Metabolic Control of Mitochondrial Transport:** Mitochondrial transport is primarily mediated by microtubule-dependent motors like kinesin. Glucose levels in synapses can influence mitochondrial transport, affecting energy consumption and signaling processes. **Metabolic Control of Mitophagy:** Mitophagy is a process that removes dysfunctional mitochondria through autophagy. The Pink1/Parkin pathway is best studied, where Pink1 accumulates on depolarized mitochondria and recruits Parkin, an E3 ligase, to ubiquitinate and target mitochondria for degradation. AMPK activation during energy stress also promotes mitophagy by activating ULK1 and ULK2, which promote autophagy. Hypoxic conditions trigger mitophagy through the dephosphorylation of FUNDC1 by PGAM5, promoting autophagic membrane formation. The review highlights the complex interplay between mitochondrial dynamics and metabolism, emphasizing the importance of understanding these processes for therapeutic interventions in diseases related to mitochondrial dysfunction.