Response of ROS under different mechanisms in cardiovascular diseases
Disease types | ROS | Mechanisms | PMIDs | Publication dates |
---|---|---|---|---|
I/R | ↑ | Ripk3–Ca2+ overload–XO–ROS | 29502045 | 2018-02 |
↓ | HIF-1–NADPH–mtROS | 34763860 | 2022-02 | |
↓ | AMPK–Akt–GSK-3β–ROS | 28128361 | 2017-01 | |
↓ | TAK1↓–ROS | 32378287 | 2020-10 | |
↓ | GJA1-20k–ROS | 34608863 | 2021-10 | |
↓ | PHLDA1–ROS | 31981628 | 2020-03 | |
Hypertension | ↓ | JMJD1A–ROS | 32461996 | 2020-05 |
↓ | AMPK–PAR1–ROS | 29287725 | 2018-01 | |
↓ | AMPK–PINK1–parkin–ROS | 29285690 | 2018-03 | |
↓ | AMPK–O-GlcNAC↓–ROS | 29285690 | 2018-01 | |
↓ | Sirt1–LKB1–MAPK–ROS | 23707558 | 2013-10 | |
↓ | Foxo1–SOD2–ROS | 30677512 | 2019-06 | |
↓ | ROS–Nrf2–ARE–ROS | 33656904 | 2020-12 | |
↑ | AngII–ROS | 30643968 | 2019-01 | |
↓ | CELF1↓–PEBP1–MAPK↓–ROS | 34669021 | 2022-01 | |
Atherosclerosis | ↓ | IRS-1–ROS | 33000267 | 2020-11 |
↑ | HIF-1–ROS | 35111045 | 2021-12 | |
↓ | PON2–ROS | 17404154 | 2007-04 | |
↑ | AMPK–NOX↓–ROS | 31331111 | 2019-07 | |
↓ | PKM2↓–G6P–NADPH–ROS | 30222136 | 2018-10 | |
↓ | Sirt3–Foxo3α–MnSOD–ROS | 23665396 | 2013-10 | |
↓ | Sirt3–IDH2–GSH–ROS | 30455381 | 2019-01 | |
DCM | ↑ | RAGE–NOX–ROS | 27916650 | 2017-04 |
↑ | PKC–NF-κB–iNOS–ROS | 27916650 | 2017-04 | |
↑ | NEU1–AMPKα↓–Sirt3↓–SOD2↓–ROS | 35002528 | 2022-01 | |
Heart failure | ↑ | Sirt3–CypD–mPTP–SOD↓–ROS | 33508434 | 2021-03 |
Vascular endothelial | ↓ | Sirt2–Foxo3α–SOD–ROS | 34028177 | 2021-07 |
AngII: angiotensin II; ARE: antioxidant response element; CELF1: cytimidine uracil guanine triplet repeat-binding protein 1; CypD: cyclophilin D; Foxo1: forkhead box protein O1; Foxo3α: forkhead box transcription factor 3α; G6P: glucose-6-phosphate; IDH2: isocitrate dehydrogenase 2; IRS-1: insulin receptor substrate 1; JMJD1A: Jumonji domain containing 1A; LKB1: liver kinase B1; MAPK: mitogen-activated protein kinases; MnSOD: manganese SOD; NEU1: neuraminidase 1; NF-κB: nuclear factor kappaB; Nrf2: nuclear factor E2-related factor 2; O-GlcNAC: O-linked N-acetylglucosamine; PAR1: protease-activated receptor 1; PEBP1: phosphatidylethanolamine binding protein 1; PINK1: phosphatase and tensin homolog-induced putative kinase 1; PKC: protein kinase C; PKM2: pyruvate kinase M2; PON2: paraoxonase-2; RAGE: receptor for advanced glycation end products; Ripk3: receptor-interacting serine/threonine-protein kinase 3; Sirt 1: sirtuin 1; PMID: PubMed ID; ↑: increase; ↓: decrease
JF, LJD and JR contributed conception and design of the study; JF and JR wrote the first draft of the manuscript. All authors contributed to manuscript revision, read and approved the submitted version.
The authors declare that they have no conflicts of interest.
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Work in our lab has been supported by the National Key R&D Program of China (2017YFA0506000). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
© The Author(s) 2022.