CoChat
Sign Up
Cited by 45

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

GOLPH3 promotes endotoxemia-induced liver and kidney injury through Golgi stress-mediated apoptosis and inflammatory response

Dusabimana, Theodomir, Je, Jihyun, Yun, Seung Pil, Kim, Hye Jung, Kim, Hwajin, Park, Sang Won·2023·Cell Death & Disease
DOI 10.1038/s41419-023-05975-xPMC PMC10361983
Open this paper in CoChat — free account

Abstract

Sepsis is a serious clinical condition characterized by a systemic inflammatory response, a leading cause of acute liver and kidney injury, and is associated with a high morbidity and mortality. Understanding the molecular mechanisms underlying the acute liver and kidney injury is crucial for developing an effective therapy. Golgi apparatus plays important roles and has various substrates mediating cellular stress responses. Golgi phosphoprotein 3 (GOLPH3), linking Golgi membranes to the cytoskeleton, has been identified as an important oncogenic regulator; however, its role in endotoxemia-induced acute liver and kidney injury remains elusive. Here, we found that upregulation of GOLPH3 was associated with endotoxemia-induced acute liver and kidney injury. Lipopolysaccharide (LPS) treatment increased Golgi stress and fragmentation, and associated pro-inflammatory mediator ( Tnfα, IL-6 , and IL-1β) production in vivo and in vitro. Interestingly, the downregulation of GOLPH3 significantly decreased LPS-induced Golgi stress and pro-inflammatory mediators ( Tnfα, IL-6, Mcp1 , and Nos2) , and reversed apoptotic cell deaths in LPS-treated hepatocytes and renal tubular cells. GOLPH3 knockdown also reduced inflammatory response in LPS-treated macrophages. The AKT/NF-kB signaling pathway was suppressed in GOLPH3 knockdown, which may be associated with a reduction of inflammatory response and apoptosis and the recovery of Golgi morphology and function. Taken together, GOLPH3 plays a crucial role in the development and progression of acute liver and kidney injury by promoting Golgi stress and increasing inflammatory response and apoptosis, suggesting GOLPH3 as a potential therapeutic target for endotoxemia-induced tissue injury.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/s41419-023-05975-x

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Show all 2 references

Research works printed but not linked: 49

  1. Nascimento DC, Melo PH, Pineros AR, Ferreira RG, Colon DF, Donate PB, et al. IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nat Commun. 2017;8:14919. · DOI
  2. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016;315:801–10. · DOI · Paper page
  3. Rudd KE, Johnson SC, Agesa KM, Shackelford KA, Tsoi D, Kievlan DR, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet 2020;395:200–11. · DOI · Paper page
  4. Ye M, Zhao Y, Wang Y, Xie R, Tong Y, Sauer JD, et al. NAD(H)-loaded nanoparticles for efficient sepsis therapy via modulating immune and vascular homeostasis. Nat Nanotechnol. 2022;17:880–90. · DOI
  5. Delano MJ, Ward PA. The immune system’s role in sepsis progression, resolution, and long-term outcome. Immunol Rev. 2016;274:330–53. · DOI · Paper page
  6. Hotchkiss RS, Moldawer LL, Opal SM, Reinhart K, Turnbull IR, Vincent JL. Sepsis and septic shock. Nat Rev Dis Prim. 2016;2:16045. · DOI
  7. Lelubre C, Vincent JL. Mechanisms and treatment of organ failure in sepsis. Nat Rev Nephrol. 2018;14:417–27. · DOI
  8. Liu Z, Tang C, He L, Yang D, Cai J, Zhu J, et al. The negative feedback loop of NF-kappaB/miR-376b/NFKBIZ in septic acute kidney injury. JCI Insight. 2020;5:e142272. · DOI
  9. Chen SN, Tan Y, Xiao XC, Li Q, Wu Q, Peng YY, et al. Deletion of TLR4 attenuates lipopolysaccharide-induced acute liver injury by inhibiting inflammation and apoptosis. Acta Pharm Sin. 2021;42:1610–9. · DOI
  10. Gomez H, Ince C, De Backer D, Pickkers P, Payen D, Hotchkiss J, et al. A unified theory of sepsis-induced acute kidney injury: inflammation, microcirculatory dysfunction, bioenergetics, and the tubular cell adaptation to injury. Shock 2014;41:3–11. · DOI
  11. Molema G, Zijlstra JG, van Meurs M, Kamps J. Renal microvascular endothelial cell responses in sepsis-induced acute kidney injury. Nat Rev Nephrol. 2022;18:95–112. · DOI
  12. Basile DP, Anderson MD, Sutton TA. Pathophysiology of acute kidney injury. Compr Physiol. 2012;2:1303–53. · DOI
  13. Silveira MAD, Capcha JMC, Sanches TR, de Sousa Moreira R, Garnica MS, Shimizu MH, et al. Green propolis extract attenuates acute kidney injury and lung injury in a rat model of sepsis. Sci Rep. 2021;11:5925. · DOI
  14. Wang B, Xu J, Ren Q, Cheng L, Guo F, Liang Y, et al. Fatty acid-binding protein 4 is a therapeutic target for septic acute kidney injury by regulating inflammatory response and cell apoptosis. Cell Death Dis. 2022;13:333. · DOI
  15. Casey CA, Thomes P, Manca S, Petrosyan A. Giantin is required for post-alcohol recovery of Golgi in liver cells. Biomolecules. 2018;8:150. · DOI
  16. Joshi G, Bekier ME 2nd, Wang Y. Golgi fragmentation in Alzheimer’s disease. Front Neurosci. 2015;9:340. · DOI
  17. Li T, You H, Zhang J, Mo X, He W, Chen Y, et al. Study of GOLPH3: a potential stress-inducible protein from Golgi apparatus. Mol Neurobiol. 2014;49:1449–59. · DOI
  18. Han H, He Y, Hu J, Lau R, Lee H, Ji C. Disrupted ER-to-Golgi trafficking underlies anti-HIV drugs and alcohol-induced cellular stress and hepatic injury. Hepatol Commun. 2017;1:122–39. · DOI
  19. Deng S, Liu J, Wu X, Lu W. Golgi apparatus: a potential therapeutic target for autophagy-associated neurological diseases. Front Cell Dev Biol. 2020;8:564975. · DOI
  20. Li J, Ahat E, Wang Y. Golgi structure and function in health, stress, and diseases. Results Probl Cell Differ. 2019;67:441–85. · DOI
  21. Makhoul C, Gosavi P, Duffield R, Delbridge B, Williamson NA, Gleeson PA. Intersectin-1 interacts with the golgin GCC88 to couple the actin network and Golgi architecture. Mol Biol Cell. 2019;30:370–86. · DOI
  22. Yang D, Yao M, Yan Y, Liu Y, Wen X, Chen X, et al. Deoxycholic acid upregulates serum Golgi protein 73 through activating NF-kappaB pathway and destroying Golgi structure in liver disease. Biomolecules. 2021;11:205. · DOI
  23. Wu S, Fu J, Dong Y, Yi Q, Lu D, Wang W, et al. GOLPH3 promotes glioma progression via facilitating JAK2-STAT3 pathway activation. J Neurooncol. 2018;139:269–79. · DOI
  24. Buschman MD, Xing M, Field SJ. The GOLPH3 pathway regulates Golgi shape and function and is activated by DNA damage. Front Neurosci. 2015;9:362. · DOI
  25. Li Y, Zhang H, Long W, Gao M, Guo W, Yu L. Inhibition of NLRP3 and Golph3 ameliorates diabetes-induced neuroinflammation in vitro and in vivo. Aging. 2022;14:8745–62. · DOI
  26. Liu H, Wang X, Feng B, Tang L, Li W, Zheng X, et al. Golgi phosphoprotein 3 (GOLPH3) promotes hepatocellular carcinoma progression by activating mTOR signaling pathway. BMC Cancer. 2018;18:661. · DOI
  27. Dai T, Zhang D, Cai M, Wang C, Wu Z, Ying Z, et al. Golgi phosphoprotein 3 (GOLPH3) promotes hepatocellular carcinoma cell aggressiveness by activating the NF-kappaB pathway. J Pathol. 2015;235:490–501. · DOI
  28. Sechi S, Frappaolo A, Belloni G, Colotti G, Giansanti MG. The multiple cellular functions of the oncoprotein Golgi phosphoprotein 3. Oncotarget 2015;6:3493–506. · DOI
  29. Li T, You H, Mo X, He W, Tang X, Jiang Z, et al. GOLPH3 mediated Golgi stress response in modulating N2A cell death upon oxygen-glucose deprivation and reoxygenation injury. Mol Neurobiol. 2016;53:1377–85. · DOI
  30. Li X, Yu J, Gong L, Zhang Y, Dong S, Shi J, et al. Heme oxygenase-1(HO-1) regulates Golgi stress and attenuates endotoxin-induced acute lung injury through hypoxia inducible factor-1alpha (HIF-1alpha)/HO-1 signaling pathway. Free Radic Biol Med. 2021;165:243–53. · DOI
  31. Kim H, Dusabimana T, Kim SR, Je J, Jeong K, Kang MC, et al. Supplementation of Abelmoschus manihot ameliorates diabetic nephropathy and hepatic steatosis by activating autophagy in mice. Nutrients. 2018;10:1703. · DOI
  32. Dusabimana T, Kim SR, Kim HJ, Park SW, Kim H. Nobiletin ameliorates hepatic ischemia and reperfusion injury through the activation of SIRT-1/FOXO3a-mediated autophagy and mitochondrial biogenesis. Exp Mol Med. 2019;51:1–16. · DOI
  33. Khader A, Yang WL, Godwin A, Prince JM, Nicastro JM, Coppa GF, et al. Sirtuin 1 stimulation attenuates ischemic liver injury and enhances mitochondrial recovery and autophagy. Crit Care Med. 2016;44:e651–63. · DOI
  34. Sureshbabu A, Patino E, Ma KC, Laursen K, Finkelsztein EJ, Akchurin O, et al. RIPK3 promotes sepsis-induced acute kidney injury via mitochondrial dysfunction. JCI Insight. 2018;3:e98411. · DOI
  35. Hu X, Xu Y, Zhang Z, Tang Z, Zhang J, Luo Y, et al. TSC1 affects the process of renal ischemia-reperfusion injury by controlling macrophage polarization. Front Immunol. 2021;12:637335. · DOI
  36. Hansen MD, Johnsen IB, Stiberg KA, Sherstova T, Wakita T, Richard GM, et al. Hepatitis C virus triggers Golgi fragmentation and autophagy through the immunity-related GTPase M. Proc Natl Acad Sci USA. 2017;114:E3462–E71. · DOI
  37. Kim H, Kim SR, Je J, Jeong K, Kim S, Kim HJ, et al. The proximal tubular alpha7 nicotinic acetylcholine receptor attenuates ischemic acute kidney injury through Akt/PKC signaling-mediated HO-1 induction. Exp Mol Med. 2018;50:1–17.
  38. Ruggiero FM, Martinez-Koteski N, Fidelio GD, Vilcaes AA, Daniotti JL. Golgi phosphoprotein 3 regulates the physical association of glycolipid glycosyltransferases. Int J Mol Sci. 2022;23:10354. · DOI
  39. Zhang X. Alterations of Golgi structural proteins and glycosylation defects in cancer. Front Cell Dev Biol. 2021;9:665289. · DOI
  40. Reiling JH, Olive AJ, Sanyal S, Carette JE, Brummelkamp TR, Ploegh HL, et al. A CREB3-ARF4 signalling pathway mediates the response to Golgi stress and susceptibility to pathogens. Nat Cell Biol. 2013;15:1473–85. · DOI · Paper page
  41. Cao Q, Harris DC, Wang Y. Macrophages in kidney injury, inflammation, and fibrosis. Physiol (Bethesda). 2015;30:183–94.
  42. Kim SR, Park EJ, Dusabimana T, Je J, Jeong K, Yun SP, et al. Platycodon grandiflorus fermented extracts attenuate endotoxin-induced acute liver injury in mice. Nutrients. 2020;12:2802. · DOI
  43. Ju C, Tacke F. Hepatic macrophages in homeostasis and liver diseases: from pathogenesis to novel therapeutic strategies. Cell Mol Immunol. 2016;13:316–27. · DOI · Paper page
  44. Hobbs S, Reynoso M, Geddis AV, Mitrophanov AY, Matheny RW Jr. LPS-stimulated NF-kappaB p65 dynamic response marks the initiation of TNF expression and transition to IL-10 expression in RAW 264.7 macrophages. Physiol Rep. 2018;6:e13914. · DOI
  45. Xue Y, Wu G, Liao Y, Xiao G, Ma X, Zou X, et al. GOLPH3 is a novel marker of poor prognosis and a potential therapeutic target in human renal cell carcinoma. Br J Cancer. 2014;110:2250–60. · DOI
  46. Zhang Y, Wang Y, Read E, Fu M, Pei Y, Wu L, et al. Golgi stress response, hydrogen sulfide metabolism, and intracellular calcium homeostasis. Antioxid Redox Signal. 2020;32:583–601. · DOI
  47. Jang J, Song J, Lee H, Sim I, Kwon YV, Jho EH, et al. LGK974 suppresses lipopolysaccharide-induced endotoxemia in mice by modulating the crosstalk between the Wnt/beta-catenin and NF-kappaB pathways. Exp Mol Med. 2021;53:407–21. · DOI
  48. Tang B, Tang F, Wang Z, Qi G, Liang X, Li B, et al. Upregulation of Akt/NF-kappaB-regulated inflammation and Akt/Bad-related apoptosis signaling pathway involved in hepatic carcinoma process: suppression by carnosic acid nanoparticle. Int J Nanomed. 2016;11:6401–20. · DOI
  49. Liu SF, Malik AB. NF-kappa B activation as a pathological mechanism of septic shock and inflammation. Am J Physiol Lung Cell Mol Physiol. 2006;290:L622–L45. · DOI

Cited by

Sorted by citations

See all 45

Metadata

Authors
Dusabimana, T., Je, J., Yun, S. P., Kim, H. J., Kim, H., & Park, S. W.
ORCID
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2023-07-21
Volume
14
Issue
7
ISSN
2041-4889
DOI
10.1038/s41419-023-05975-x
PMC
PMC10361983
Cited by
45
References
2
Language
en
Licence
Funders
National Research Foundation of Korea (2021R1A5A8029490, 2020R1A2C1014739, 2021R1A2C1010685)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review