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Mature neurons typically fail to regenerate after injury, thus raising a fundamental question as to whether mitochondrial transport is necessary to meet enhanced metabolic requirements during regeneration. Here, we reveal that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms controlling regrowth in mature neurons. Axotomy induces acute mitochondrial depolarization and ATP depletion in injured axons. Thus, mature neuron-associated increases in mitochondria-anchoring protein syntaphilin (SNPH) and decreases in mitochondrial transport cause local energy deficits. Strikingly, enhancing mitochondrial transport via genetic manipulation facilitates regenerative capacity by replenishing healthy mitochondria in injured axons, thereby rescuing energy deficits. An in vivo sciatic nerve crush study further shows that enhanced mitochondrial transport in snph knockout mice accelerates axon regeneration. Understanding deficits in mitochondrial trafficking and energy supply in injured axons of mature neurons benefits development of new strategies to stimulate axon regeneration.<\/jats:p>","DOI":"10.1083\/jcb.201605101","type":"journal-article","created":{"date-parts":[[2016,6,8]],"date-time":"2016-06-08T11:06:19Z","timestamp":1465383979000},"page":"103-119","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":315,"title":["Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits"],"prefix":"10.1083","volume":"214","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7718-2311","authenticated-orcid":false,"given":"Bing","family":"Zhou","sequence":"first","affiliation":[{"name":"Synaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Panpan","family":"Yu","sequence":"additional","affiliation":[{"name":"Guangdong\u2013Hong Kong\u2013Macau Institute of CNS Regeneration, Ministry of Education Joint International Research Laboratory of CNS Regeneration, Jinan University, Guangzhou 510632, China 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei-Yao","family":"Lin","sequence":"additional","affiliation":[{"name":"Synaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7834-0721","authenticated-orcid":false,"given":"Tao","family":"Sun","sequence":"additional","affiliation":[{"name":"Synaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanmin","family":"Chen","sequence":"additional","affiliation":[{"name":"Synaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zu-Hang","family":"Sheng","sequence":"additional","affiliation":[{"name":"Synaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 1"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2016,6,7]]},"reference":[{"key":"2023072308523661500_bib1","doi-asserted-by":"publisher","first-page":"276","DOI":"10.1016\/j.conb.2008.06.005","article-title":"Nerve injury signaling","volume":"18","author":"Abe","year":"2008","journal-title":"Curr. 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