[1] |
AMERICAN DIABETES ASSOCIATION. 11. microvascular complications and foot care:standards of medical care in diabetes-2021[J]. Diabetes Care, 2021, 44(Suppl 1):S151-167. DOI: 10.2337/dc21-S011.
|
[2] |
SOYOYE D O, ABIODUN O O, IKEM R T,et al. Diabetes and peripheral artery disease:a review[J]. World J Diabetes, 2021, 12(6):827-838. DOI: 10.4239/wjd.v12.i6.827.
|
[3] |
EISINGER F, PATZELT J, LANGER H F. The platelet response to tissue injury[J]. Front Med (Lausanne), 2018, 5:317. DOI: 10.3389/fmed.2018.00317.
|
[4] |
|
[5] |
TIAN M, QING C, NIU Y W,et al. The relationship between inflammation and impaired wound healing in a diabetic rat burn model[J]. J Burn Care Res, 2016, 37(2):e115-124. DOI: 10.1097/BCR.0000000000000171.
|
[6] |
PASTAR I, STOJADINOVIC O, YIN N C,et al. Epithelialization in wound healing:a comprehensive review[J]. Adv Wound Care (New Rochelle), 2014, 3(7):445-464. DOI: 10.1089/wound.2013.0473.
|
[7] |
ARYA A K, TRIPATHI R, KUMAR S,et al. Recent advances on the association of apoptosis in chronic non healing diabetic wound[J]. World J Diabetes, 2014, 5(6):756-762. DOI: 10.4239/wjd.v5.i6.756.
|
[8] |
KHALID M, PETROIANU G, ADEM A. Advanced glycation end products and diabetes mellitus:mechanisms and perspectives[J]. Biomolecules, 2022, 12(4):542. DOI: 10.3390/biom12040542.
|
[9] |
WILGUS T A, ROY S, MCDANIEL J C. Neutrophils and wound repair:positive actions and negative reactions[J]. Adv Wound Care (New Rochelle), 2013, 2(7):379-388. DOI: 10.1089/wound.2012.0383.
|
[10] |
MOOR A N, VACHON D J, GOULD L J. Proteolytic activity in wound fluids and tissues derived from chronic venous leg ulcers[J]. Wound Repair Regen, 2009, 17(6):832-839. DOI: 10.1111/j.1524-475X.2009.00547.x.
|
[11] |
DAS A, GANESH K, KHANNA S,et al. Engulfment of apoptotic cells by macrophages:a role of microRNA-21 in the resolution of wound inflammation[J]. J Immunol, 2014, 192(3):1120-1129. DOI: 10.4049/jimmunol.1300613.
|
[12] |
PAREDES L C, LUZ R B D S, TOZZI O N,et al. Distinct macrophage phenotypes and redox environment during the fin fold regenerative process in zebrafish[J]. Scand J Immunol, 2021, 94(2):e13026. DOI: 10.1111/sji.13026.
|
[13] |
|
[14] |
NWOMEH B C, LIANG H X, DIEGELMANN R F,et al. Dynamics of the matrix metalloproteinases MMP-1 and MMP-8 in acute open human dermal wounds[J]. Wound Repair Regen, 1998, 6(2):127-134. DOI: 10.1046/j.1524-475x.1998.60206.x.
|
[15] |
KHANNA S, BISWAS S, SHANG Y L,et al. Macrophage dysfunction impairs resolution of inflammation in the wounds of diabetic mice[J]. PLoS One, 2010, 5(3):e9539. DOI: 10.1371/journal.pone.0009539.
|
[16] |
WANG Q, ZHU G Y, CAO X Z,et al. Blocking AGE-RAGE signaling improved functional disorders of macrophages in diabetic wound[J]. J Diabetes Res, 2017, 2017:1428537. DOI: 10.1155/2017/1428537.
|
[17] |
AITCHESON S M, FRENTIU F D, HURN S E,et al. Skin wound healing:normal macrophage function and macrophage dysfunction in diabetic wounds[J]. Molecules, 2021, 26(16):4917. DOI: 10.3390/molecules26164917.
|
[18] |
PINTO-JUNIOR D C, SILVA K S, MICHALANI M L,et al. Advanced glycation end products-induced insulin resistance involves repression of skeletal muscle GLUT4 expression[J]. Sci Rep, 2018, 8(1):8109. DOI: 10.1038/s41598-018-26482-6.
|
[19] |
LARTIGUE L, FAUSTIN B. Mitochondria:metabolic regulators of innate immune responses to pathogens and cell stress[J]. Int J Biochem Cell Biol, 2013, 45(9):2052-2056. DOI: 10.1016/j.biocel.2013.06.014.
|
[20] |
ROSSIGNOL R,LETELLIER T,MALGAT M,et al. Tissue variation in the control of oxidative phosphorylation:implication for mitochondrial diseases[J]. Biochem J,2000,347(Pt 1):45-53.
|
[21] |
GÓMEZ-VALADES A G, GONZALEZ-FRANQUESA A, GAMA-PEREZ P,et al. Emerging concepts in diabetes:mitochondrial dynamics and glucose homeostasis[J]. Curr Diabetes Rev, 2017, 13(4):370-385. DOI: 10.2174/1573399812666151012115229.
|
[22] |
CHOO H J, KIM J H, KWON O B,et al. Mitochondria are impaired in the adipocytes of type 2 diabetic mice[J]. Diabetologia, 2006, 49(4):784-791. DOI: 10.1007/s00125-006-0170-2.
|
[23] |
PINTI M V, FINK G K, HATHAWAY Q A,et al. Mitochondrial dysfunction in type 2 diabetes mellitus:an organ-based analysis[J]. Am J Physiol Endocrinol Metab, 2019, 316(2):E268-285. DOI: 10.1152/ajpendo.00314.2018.
|
[24] |
RIEUSSET J. Contribution of mitochondria and endoplasmic Reticulum dysfunction in insulin resistance:distinct or interrelated roles? [J]. Diabetes Metab, 2015, 41(5):358-368. DOI: 10.1016/j.diabet.2015.02.006.
|
[25] |
CHATTOPADHYAY M, KHEMKA V K, CHATTERJEE G,et al. Enhanced ROS production and oxidative damage in subcutaneous white adipose tissue mitochondria in obese and type 2 diabetes subjects[J]. Mol Cell Biochem, 2015, 399(1/2):95-103. DOI: 10.1007/s11010-014-2236-7.
|
[26] |
ANDERSON E J, LUSTIG M E, BOYLE K E,et al. Mitochondrial H 2O 2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans[J]. J Clin Invest, 2009, 119(3):573-581. DOI: 10.1172/JCI37048.
|
[27] |
OTT M, GOGVADZE V, ORRENIUS S,et al. Mitochondria,oxidative stress and cell death[J]. Apoptosis, 2007, 12(5):913-922. DOI: 10.1007/s10495-007-0756-2.
|
[28] |
MURPHY M P. How mitochondria produce reactive oxygen species[J]. Biochem J, 2009, 417(1):1-13. DOI: 10.1042/BJ20081386.
|
[29] |
ZHANG B Y, PAN C Y, FENG C,et al. Role of mitochondrial reactive oxygen species in homeostasis regulation[J]. Redox Rep, 2022, 27(1):45-52. DOI: 10.1080/13510002.2022.2046423.
|
[30] |
KOENIG A, BUSKIEWICZ-KOENIG I A. Redox activation of mitochondrial DAMPs and the metabolic consequences for development of autoimmunity[J]. Antioxid Redox Signal, 2022, 36(7/8/9):441-461. DOI: 10.1089/ars.2021.0073.
|
[31] |
BRAND M D, AFFOURTIT C, ESTEVES T C,et al. Mitochondrial superoxide:production,biological effects,and activation of uncoupling proteins[J]. Free Radic Biol Med, 2004, 37(6):755-767. DOI: 10.1016/j.freeradbiomed.2004.05.034.
|
[32] |
KRYSKO D V, AGOSTINIS P, KRYSKO O,et al. Emerging role of damage-associated molecular patterns derived from mitochondria in inflammation[J]. Trends Immunol, 2011, 32(4):157-164. DOI: 10.1016/j.it.2011.01.005.
|
[33] |
XIE L L, SHI F, TAN Z Q,et al. Mitochondrial network structure homeostasis and cell death[J]. Cancer Sci, 2018, 109(12):3686-3694. DOI: 10.1111/cas.13830.
|
[34] |
GOTTLIEB R A, PIPLANI H, SIN J,et al. At the heart of mitochondrial quality control:many roads to the top[J]. Cell Mol Life Sci, 2021, 78(8):3791-3801. DOI: 10.1007/s00018-021-03772-3.
|
[35] |
|
[36] |
HASSON S A, KANE L A, YAMANO K,et al. High-content genome-wide RNAi screens identify regulators of parkin upstream of mitophagy[J]. Nature, 2013, 504(7479):291-295. DOI: 10.1038/nature12748.
|
[37] |
ROJANSKY R, CHA M Y, CHAN D C. Elimination of paternal mitochondria in mouse embryos occurs through autophagic degradation dependent on PARKIN and MUL1[J]. eLife, 2016, 5:e17896. DOI: 10.7554/eLife.17896.
|
[38] |
GAN Z Y, CALLEGARI S, COBBOLD S A,et al. Activation mechanism of PINK1[J]. Nature, 2022, 602(7896):328-335. DOI: 10.1038/s41586-021-04340-2.
|
[39] |
NARENDRA D, TANAKA A, SUEN D F,et al. Parkin is recruited selectively to impaired mitochondria and promotes their autophagy[J]. J Cell Biol, 2008, 183(5):795-803. DOI: 10.1083/jcb.200809125.
|
[40] |
MCWILLIAMS T G, MUQIT M M. PINK1 and Parkin:emerging themes in mitochondrial homeostasis[J]. Curr Opin Cell Biol, 2017, 45:83-91. DOI: 10.1016/j.ceb.2017.03.013.
|
[41] |
LAZAROU M, SLITER D A, KANE L A,et al. The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy[J]. Nature, 2015, 524(7565):309-314. DOI: 10.1038/nature14893.
|
[42] |
ARENA G, GELMETTI V, TOROSANTUCCI L,et al. PINK1 protects against cell death induced by mitochondrial depolarization,by phosphorylating Bcl-xL and impairing its pro-apoptotic cleavage[J]. Cell Death Differ, 2013, 20(7):920-930. DOI: 10.1038/cdd.2013.19.
|
[43] |
ARENA G, VALENTE E M. PINK1 in the limelight:multiple functions of an eclectic protein in human health and disease[J]. J Pathol, 2017, 241(2):251-263. DOI: 10.1002/path.4815.
|
[44] |
CHOI J, RAVIPATI A, NIMMAGADDA V,et al. Potential roles of PINK1 for increased PGC-1α-mediated mitochondrial fatty acid oxidation and their associations with Alzheimer disease and diabetes[J]. Mitochondrion, 2014, 18:41-48. DOI: 10.1016/j.mito.2014.09.005.
|
[45] |
MARTELLA G, MADEO G, MALTESE M,et al. Exposure to low-dose rotenone precipitates synaptic plasticity alterations in PINK1 heterozygous knockout mice[J]. Neurobiol Dis, 2016, 91:21-36. DOI: 10.1016/j.nbd.2015.12.020.
|
[46] |
AKUNDI R S, ZHI L T, SULLIVAN P G,et al. Shared and cell type-specific mitochondrial defects and metabolic adaptations in primary cells from PINK1-deficient mice[J]. Neurodegener Dis, 2013, 12(3):136-149. DOI: 10.1159/000345689.
|
[47] |
KOH H, CHUNG J. PINK1 as a molecular checkpoint in the maintenance of mitochondrial function and integrity[J]. Mol Cells, 2012, 34(1):7-13. DOI: 10.1007/s10059-012-0100-8.
|
[48] |
VALENTE E M, ABOU-SLEIMAN P M, CAPUTO V,et al. Hereditary early-onset Parkinson's disease caused by mutations in PINK1[J]. Science, 2004, 304(5674):1158-1160. DOI: 10.1126/science.1096284.
|
[49] |
DEAS E, PIIPARI K, MACHHADA A,et al. PINK1 deficiency in β-cells increases basal insulin secretion and improves glucose tolerance in mice[J]. Open Biol, 2014, 4:140051. DOI: 10.1098/rsob.140051.
|
[50] |
CANG X M, WANG X H, LIU P L,et al. PINK1 alleviates palmitate induced insulin resistance in HepG2 cells by suppressing ROS mediated MAPK pathways[J]. Biochem Biophys Res Commun, 2016, 478(1):431-438. DOI: 10.1016/j.bbrc.2016.07.004.
|
[51] |
BHANSALI S, BHANSALI A, WALIA R,et al. Alterations in mitochondrial oxidative stress and mitophagy in subjects with prediabetes and type 2 diabetes mellitus[J]. Front Endocrinol (Lausanne), 2017, 8:347. DOI: 10.3389/fendo.2017.00347.
|
[52] |
LIU K, ZHAO E P, ILYAS G,et al. Impaired macrophage autophagy increases the immune response in obese mice by promoting proinflammatory macrophage polarization[J]. Autophagy, 2015, 11(2):271-284. DOI: 10.1080/15548627.2015.1009787.
|
[53] |
LIN Q S, LI S, JIANG N,et al. PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation[J]. Redox Biol, 2019, 26:101254. DOI: 10.1016/j.redox.2019.101254.
|
[54] |
ZHANG Y, SAULER M, SHINN A S,et al. Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury[J]. J Immunol, 2014, 192(11):5296-5304. DOI: 10.4049/jimmunol.1400653.
|
[55] |
QASIM W, LI Y, SUN R M,et al. PTEN-induced kinase 1-induced dynamin-related protein 1 Ser637 phosphorylation reduces mitochondrial fission and protects against intestinal ischemia reperfusion injury[J]. World J Gastroenterol, 2020, 26(15):1758-1774. DOI: 10.3748/wjg.v26.i15.1758.
|
[56] |
MURATA H, TAKAMATSU H, LIU S L,et al. NRF2 regulates PINK1 expression under oxidative stress conditions[J]. PLoS One, 2015, 10(11):e0142438. DOI: 10.1371/journal.pone.0142438.
|
[57] |
MEI Y, ZHANG Y R, YAMAMOTO K,et al. FOXO3a-dependent regulation of Pink1 (Park6) mediates survival signaling in response to cytokine deprivation[J]. Proc Natl Acad Sci USA, 2009, 106(13):5153-5158. DOI: 10.1073/pnas.0901104106.
|
[58] |
JULIANA C, FERNANDES-ALNEMRI T, KANG S,et al. Non-transcriptional priming and deubiquitination regulate NLRP3 inflammasome activation[J]. J Biol Chem, 2012, 287(43):36617-36622. DOI: 10.1074/jbc.M112.407130.
|
[59] |
SHIMADA K, CROTHER T R, KARLIN J,et al. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis[J]. Immunity, 2012, 36(3):401-414. DOI: 10.1016/j.immuni.2012.01.009.
|
[60] |
BAUERNFEIND F, BARTOK E, RIEGER A,et al. Cutting edge:reactive oxygen species inhibitors block priming,but not activation,of the NLRP3 inflammasome[J]. J Immunol, 2011, 187(2):613-617. DOI: 10.4049/jimmunol.1100613.
|
[61] |
SWANSON K V, DENG M, TING J P Y. The NLRP3 inflammasome:molecular activation and regulation to therapeutics[J]. Nat Rev Immunol, 2019, 19(8):477-489. DOI: 10.1038/s41577-019-0165-0.
|
[62] |
KANKI T, FURUKAWA K, YAMASHITA S I. Mitophagy in yeast:molecular mechanisms and physiological role[J]. Biochim Biophys Acta, 2015, 1853(10 Pt B):2756-2765. DOI: 10.1016/j.bbamcr.2015.01.005.
|
[63] |
ZHOU R B, YAZDI A S, MENU P,et al. A role for mitochondria in NLRP3 inflammasome activation[J]. Nature, 2011, 469(7329):221-225. DOI: 10.1038/nature09663.
|
[64] |
MOUTON-LIGER F, ROSAZZA T, SEPULVEDA-DIAZ J,et al. Parkin deficiency modulates NLRP3 inflammasome activation by attenuating an A20-dependent negative feedback loop[J]. Glia, 2018, 66(8):1736-1751. DOI: 10.1002/glia.23337.
|
[65] |
XU Y, TANG Y B, LU J W,et al. PINK1-mediated mitophagy protects against hepatic ischemia/reperfusion injury by restraining NLRP3 inflammasome activation[J]. Free Radic Biol Med, 2020, 160:871-886. DOI: 10.1016/j.freeradbiomed.2020.09.015.
|
[66] |
KANG R, ZENG L, XIE Y C,et al. A novel PINK1- and PARK2-dependent protective neuroimmune pathway in lethal Sepsis[J]. Autophagy, 2016, 12(12):2374-2385. DOI: 10.1080/15548627.2016.1239678.
|
[67] |
ZHANG J, HUANG W G, HE Q K,et al. PINK1/PARK2 dependent mitophagy effectively suppresses NLRP3 inflammasome to alleviate acute pancreatitis[J]. Free Radic Biol Med, 2021, 166:147-164. DOI: 10.1016/j.freeradbiomed.2021.02.019.
|
[68] |
LOWELL B B, SHULMAN G I. Mitochondrial dysfunction and type 2 diabetes[J]. Science, 2005, 307(5708):384-387. DOI: 10.1126/science.1104343.
|
[69] |
ZHANG S R,GAO Y,WANG J A. Advanced glycation end products influence mitochondrial fusion-fission dynamics through RAGE in human aortic endothelial cells[J]. Int J Clin Exp Pathol,2017,10(7):8010-8022.
|
[70] |
WU W W, XU H, WANG Z M,et al. PINK1-parkin-mediated mitophagy protects mitochondrial integrity and prevents metabolic stress-induced endothelial injury[J]. PLoS One, 2015, 10(7):e0132499. DOI: 10.1371/journal.pone.0132499.
|
[71] |
YANG J, SUN M J, CHENG R,et al. Pitavastatin activates mitophagy to protect EPC proliferation through a calcium-dependent CAMK1-PINK1 pathway in atherosclerotic mice[J]. Commun Biol, 2022, 5(1):124. DOI: 10.1038/s42003-022-03081-w.
|
[72] |
XI J X, RONG Y Z, ZHAO Z F,et al. Scutellarin ameliorates high glucose-induced vascular endothelial cells injury by activating PINK1/Parkin-mediated mitophagy[J]. J Ethnopharmacol, 2021, 271:113855. DOI: 10.1016/j.jep.2021.113855.
|
[73] |
ZHANG Y K, WANG S Y, CHEN X,et al. Liraglutide prevents high glucose induced HUVECs dysfunction via inhibition of PINK1/Parkin-dependent mitophagy[J]. Mol Cell Endocrinol, 2022, 545:111560. DOI: 10.1016/j.mce.2022.111560.
|
[74] |
XIANG J, ZHANG C L, DI T T,et al. Salvianolic acid B alleviates diabetic endothelial and mitochondrial dysfunction by down-regulating apoptosis and mitophagy of endothelial cells[J]. Bioengineered, 2022, 13(2):3486-3502. DOI: 10.1080/21655979.2022.2026552.
|
[75] |
FAN Y Z, CHENG Z L, MAO L J,et al. PINK1/TAX1BP1-directed mitophagy attenuates vascular endothelial injury induced by copper oxide nanoparticles[J]. J Nanobiotechnology, 2022, 20(1):149. DOI: 10.1186/s12951-022-01338-4.
|
[76] |
KLINKENBERG M, THUROW N, GISPERT S,et al. Enhanced vulnerability of PARK6 patient skin fibroblasts to apoptosis induced by proteasomal stress[J]. Neuroscience, 2010, 166(2):422-434. DOI: 10.1016/j.neuroscience.2009.12.068.
|
[77] |
QIANG L, YANG S, CUI Y H,et al. Keratinocyte autophagy enables the activation of keratinocytes and fibroblastsand facilitates wound healing[J]. Autophagy, 2021, 17(9):2128-2143. DOI: 10.1080/15548627.2020.1816342.
|
[78] |
MIGNEAULT F, HÉBERT M J. Autophagy,tissue repair,and fibrosis:a delicate balance[J]. Matrix Biol, 2021, 100/101:182-196. DOI: 10.1016/j.matbio.2021.01.003.
|
[79] |
ZHU W Z, YUAN Y J, LIAO G N,et al. Mesenchymal stem cells ameliorate hyperglycemia-induced endothelial injury through modulation of mitophagy[J]. Cell Death Dis, 2018, 9(8):837. DOI: 10.1038/s41419-018-0861-x.
|