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pubmed, article, google, scholar, cas, mitochondrial, chen, central, zhou, injury, res, wang, cardiac, mitophagy, fission, zhu, cell, basic, cardiol, zhang, httpsdoiorgs, microvascular, ren, nra, reperfusion, apoptosis, ischemiareperfusion, liu, data, ischemia, kinase, signal, httpsdoiorgjcellsig, death, melatonin, function, jin, myocardial, yang, pineal, httpsdoiorgjpi, biol, role, shi, research, involved, acute, activation, access, pathway,

Topics {✒️}

mitochondrial fission-vdac1-hk2-mptp-mitophagy axis governing cofilin/f-actin/lamellipodium axis st-segment-elevation myocardial infarction adipose-derived stem cells nr4a1/dna-pkcs/p53 pathway jnk/bnip3/serca/camkii pathways pi3k/akt-sfrp2 pathways month download article/chapter cardiac ischemia-reperfusion injury cardiac ischemia/reperfusion injury mff-required mitochondrial fission ppargamma/fundc1/mitophagy pathways mapk/erk signaling pathway ck2α-disturbed mitochondrial homeostasis lipid-induced mitochondrial dysfunction suppressing fundc1-mediated mitophagy mros-mediated cardiolipin oxidation ck2alpha-disturbed mitochondrial homeostasis nbcn1 sodium/bicarbonate cotransporter cardiac odorant receptor article basic research cardiac ir injury van der wal sirt1-mediated mfn1 stabilization fundc1-related mitophagy mitochondrial fission factor acute myocardial ischemia fundc1-required mitophagy ischemia/reperfusion injury full article pdf bnip3-related mitophagy acute microvascular injury chymase mediates injury erk-creb pathway acute ischemia/reperfusion cardioprotective kinase signaling protein kinase cepsilon reperfusion injury possibly hexosamine biosynthetic pathway induced mitochondrial swelling stress-induced hyperacetylation oxidative stress injury upstream regulatory mechanism hypothalamic stat3 acetylation fatal mitochondrial fission protein kinase ck2 privacy choices/manage cookies breast cancer cells provoked microvascular dysfunction melatonin-induced increase

Questions {❓}

• Meggio F, Pinna LA (2003) One-thousand-and-one substrates of protein kinase CK2?

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         headline:RETRACTED ARTICLE: NR4A1 aggravates the cardiac microvascular ischemia reperfusion injury through suppressing FUNDC1-mediated mitophagy and promoting Mff-required mitochondrial fission by CK2α
         description:Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice. Functional studies illustrated that IR injury increased NR4A1 expression, which activated serine/threonine kinase casein kinase2 α (CK2α). CK2α promoted phosphorylation of mitochondrial fission factor (Mff) and FUN14 domain-containing 1 (FUNDC1). Phosphorylated activation of Mff enhanced the cytoplasmic translocation of Drp1 to the mitochondria, leading to fatal mitochondrial fission. Excessive fission disrupted mitochondrial function and structure, ultimately triggering mitochondrial apoptosis. In addition, phosphorylated inactivation of FUNDC1 failed to launch the protective mitophagy process, resulting in the accumulation of damaged mitochondria and endothelial apoptosis. By facilitating Mff-mediated mitochondrial fission and FUNDC1-required mitophagy, NR4A1 disturbed mitochondrial homeostasis, enhanced endothelial apoptosis and provoked microvascular dysfunction. In summary, our data illustrated that NR4A1 serves as a novel culprit factor in cardiac microvascular IR injury that operates through synchronous elevation of fission and suppression of mitophagy. Novel therapeutic strategies targeting the balance among NR4A1, fission and mitophagy might provide survival advantage to microvasculature following IR stress.
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      headline:RETRACTED ARTICLE: NR4A1 aggravates the cardiac microvascular ischemia reperfusion injury through suppressing FUNDC1-mediated mitophagy and promoting Mff-required mitochondrial fission by CK2α
      description:Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice. Functional studies illustrated that IR injury increased NR4A1 expression, which activated serine/threonine kinase casein kinase2 α (CK2α). CK2α promoted phosphorylation of mitochondrial fission factor (Mff) and FUN14 domain-containing 1 (FUNDC1). Phosphorylated activation of Mff enhanced the cytoplasmic translocation of Drp1 to the mitochondria, leading to fatal mitochondrial fission. Excessive fission disrupted mitochondrial function and structure, ultimately triggering mitochondrial apoptosis. In addition, phosphorylated inactivation of FUNDC1 failed to launch the protective mitophagy process, resulting in the accumulation of damaged mitochondria and endothelial apoptosis. By facilitating Mff-mediated mitochondrial fission and FUNDC1-required mitophagy, NR4A1 disturbed mitochondrial homeostasis, enhanced endothelial apoptosis and provoked microvascular dysfunction. In summary, our data illustrated that NR4A1 serves as a novel culprit factor in cardiac microvascular IR injury that operates through synchronous elevation of fission and suppression of mitophagy. Novel therapeutic strategies targeting the balance among NR4A1, fission and mitophagy might provide survival advantage to microvasculature following IR stress.
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