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Wong Education Foundation"},{"name":"Fundamental Research Funds for the Central Universities","award":["11625112"],"award-info":[{"award-number":["11625112"]}]}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Transl Neurodegener"],"abstract":"Abstract<\/jats:title>\n \n In vitro studies have established that PTEN-induced putative kinase 1 (PINK1) and parkin are central regulators of mitophagy, and loss-of-function mutations in either gene can cause early-onset Parkinson\u2019s disease (PD). Although various animal models, including\u00a0mice and pigs with\n PINK1<\/jats:italic>\n or\n PRKN<\/jats:italic>\n knockout, have largely failed to recapitulate the neurodegeneration seen in PD patients, effective knockdown of\n PINK1<\/jats:italic>\n or\n PRKN<\/jats:italic>\n in non-human primates, when achieving substantial protein depletion, does induce dopaminergic neuron loss in the substantia nigra and \u03b1\u2011synuclein pathology, suggesting that both the degree of protein loss and the species-dependent PINK1\u2013parkin axis activity contribute to PD pathogenesis. This review compares pathological and behavioral outcomes of PINK1- and parkin-deficient animal models across species, illustrates diverse functions of the PINK1\u2013parkin axis beyond mitophagy, discusses mechanisms underlying the species-dependent differences, and highlights the therapeutic potential of targeting this pathway. The review also underscores the necessity of considering species-specific mechanisms when investigating the PINK1\/parkin pathway.\n <\/jats:p>","DOI":"10.1186\/s40035-026-00586-w","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T02:34:10Z","timestamp":1789698850000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Species-dependent activities of the PINK1\u2013parkin axis"],"prefix":"10.1186","volume":"15","author":[{"given":"Wei","family":"Huang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kecheng","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiayi","family":"Wen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tong","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shihua","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao-Jiang","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weili","family":"Yang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,18]]},"reference":[{"issue":"7","key":"586_CR1","doi-asserted-by":"publisher","first-page":"435","DOI":"10.1038\/nrn.2017.62","volume":"18","author":"AHV Schapira","year":"2017","unstructured":"Schapira AHV, Chaudhuri KR, Jenner P. 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