{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T16:08:39Z","timestamp":1785946119098,"version":"3.56.0"},"reference-count":60,"publisher":"MDPI AG","issue":"2","license":[{"start":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T00:00:00Z","timestamp":1768176000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"the National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["31972898"],"award-info":[{"award-number":["31972898"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Parkinson\u2019s disease (PD) is a neurodegenerative disorder characterized by age-dependent degeneration of dopaminergic neurons in the substantia nigra, a process mediated by \u03b1-synuclein aggregation, mitochondrial dysfunction, and impaired proteostasis. While BAP31\u2014an endoplasmic reticulum protein critical for protein trafficking and degradation\u2014has been implicated in neuronal processes, its role in PD pathogenesis remains poorly understood. To investigate the impact of BAP31 deficiency on PD progression, we generated dopamine neuron-specific BAP31 conditional knockout with DAT-Cre (cKO) mice (Slc6a3cre-BAP31fl\/fl) and subjected them to MPTP-lesioned Parkinsonian models. Compared to BAP31fl\/fl controls, Slc6a3cre-BAP31fl\/fl mice exhibited exacerbated motor deficits following MPTP treatment, including impaired rotarod performance, reduced balance beam traversal time, and diminished climbing and voluntary motor capacity abilities. BAP31 conditional deletion showed no baseline phenotype, with deficits emerging only after MPTP. Our results indicate that these behavioral impairments correlated with neuropathological hallmarks: decreased NeuN neuronal counts, elevated GFAP astrogliosis, reduced tyrosine hydroxylase levels in the substantia nigra, and aggravated dopaminergic neurodegeneration. Mechanistically, BAP31 deficiency disrupted mitochondrial homeostasis by suppressing the PINK1\u2013Parkin mitophagy pathway. Further analysis revealed that BAP31 regulates PINK1 transcription via the transcription factor Engrailed Homeobox 1. Collectively, our findings identify BAP31 as a neuroprotective modulator that mitigates PD-associated motor dysfunction by preserving mitochondrial stability, underscoring its therapeutic potential as a target for neurodegenerative disorders.<\/jats:p>","DOI":"10.3390\/cells15020137","type":"journal-article","created":{"date-parts":[[2026,1,13]],"date-time":"2026-01-13T08:17:32Z","timestamp":1768292252000},"page":"137","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["BAP31 Modulates Mitochondrial Homeostasis Through PINK1\/Parkin Pathway in MPTP Parkinsonism Mouse Models"],"prefix":"10.3390","volume":"15","author":[{"given":"Wanting","family":"Zhang","sequence":"first","affiliation":[{"name":"College of Life Science and Health, Northeastern University, Shenyang 110169, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shihao","family":"Meng","sequence":"additional","affiliation":[{"name":"College of Life Science and Health, Northeastern University, Shenyang 110169, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenzhen","family":"Hao","sequence":"additional","affiliation":[{"name":"College of Life Science and Health, Northeastern University, Shenyang 110169, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoshuang","family":"Zhu","sequence":"additional","affiliation":[{"name":"College of Life Science and Health, Northeastern University, Shenyang 110169, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lingwei","family":"Cao","sequence":"additional","affiliation":[{"name":"Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Yuan","sequence":"additional","affiliation":[{"name":"Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6549-8837","authenticated-orcid":false,"given":"Bing","family":"Wang","sequence":"additional","affiliation":[{"name":"College of Life Science and Health, Northeastern University, Shenyang 110169, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,1,12]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Chiaro, G., Vichayanrat, E., Koay, S., Rogeau, A., Ingle, G.T., McNamara, P., Watson, L., Bomanji, J., Mathias, C.J., and Iodice, V. 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