Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury
Abstract
:1. Introduction
2. Extracellular Vesicles
2.1. Nomenclature and Biogenesis
2.2. EV Characterization
2.3. Uptake and Function
2.4. Vs and MI
3. Cardiovascular Risk Factors
3.1. Diabetes Mellitus and Obesity
3.1.1. DM Type 1
3.1.2. DM Type 2 and Obesity
Increased | |||||
---|---|---|---|---|---|
miRNA | Ob | DM2 | Ref. | Effect | The Potential Regulatory Mechanism in IRI |
miR-15b | Up | - | [136,173,174,175] | Aggravating | Increases apoptosis via downregulation of Bcl-2, MAPK3, and KCNJ2 [176,177,178]; inhibits the activity of the JAK2-STAT3 pathway, and promotes ROS production [179]. |
miR-23 | Up | Up | [132,160] | Aggravating | Regulates glutamine metabolism, promotes the transformation of BMSCs into myocardial cells, suppresses expression of Manganese superoxide dismutase, enhances mitophagy, and inhibits connexin 43 expression [161,163,180,181]. |
miR-34 | Up | Up | [91,136,173,182,183] | Aggravating | Increases apoptosis, infarct size, and suppresses angiogenesis silencing sirtuin-1 and Wnt/β-catenin signaling pathway, suppresses cardiomyocyte proliferation and cardiac recovery post-MI regulating cell cycle activity and death via modulation of its targets, including Bcl2, Cyclin D1, and SIRT1 [90,91,184,185,186,187,188]. |
miR-122 | Up | Up | [132,136,173,189,190] | Aggravating | Promotes cardiomyocyte apoptosis via regulation of caspase 8 [191], inhibits the expression of Bcl-2, and upregulates the expression of HIF-1α, Bax, and caspase 9 via suppression of FOXP2 [192], downregulates the expression of the AKT/mTOR pathway, and upregulates the JNK/p38MAPK pathway [193]. |
miR-130 | Up * | Up | [68,105,132,136,173,174,194,195,196] | Aggravating | Promotes worse cardiac function recovery, larger infarct size, and greater cardiomyocyte apoptosis targeting AMPKα1/α2, Birc6, and Ucp3 [68], increases NFκB-mediated inflammation and TGF-β1-mediated fibrosis via inhibition of PPAR-γ expression [197]. |
miR-155 | Up | Up | [38,102,131,135,136,173] | Aggravating | Increases cardiomyocyte apoptosis in vitro via the downregulation of HIF-1α, RNA-binding protein Quaking, and SIRT1 [153,154,198], enhances the inflammatory response through the activation of the JAK2/STAT1 pathway [155], increases ROS generation during IRI [199]. |
miR-192 | Up | Up | [132,136,160,173,200,201] | Aggravating | Induces apoptosis targeting FABP3, regulates oxidative stress in IRI [162,202] |
miR-320 | Up | Up | [37,132,135,200] | Aggravating | Increases infarct size and promotes apoptosis via the inhibition of AKIP1, IGF-1, HSP20, and AKT3 [137,138,139,203]. |
miR-483 | Up | Up | [132,204,205] | Aggravating | Decreases cell viability and increases apoptosis by targeting the MDM4/p53 pathway [206], promotes apoptosis via the IGF-1 signaling pathway [207,208]. |
miR-21 | Up * | Up * | [38,91,132,136,173,209,210] | Attenuating | Increases angiogenesis via silencing the cell death-inducing p53 target protein 1 [211], inhibits apoptosis via p38 downregulation and PI3k/Akt activation, decreases autophagy in the myocardial tissue via the AKT/mTOR pathway [91,152,212,213,214,215,216,217]. |
miR-26b | Up | Up | [132,136,174,196,218] | Attenuating | Reduces inflammation in IRI and improves myocardial remodeling via MAPK pathway activation [219], targets High Mobility Group AT-Hook 2 suppressing MI-induced fibrosis [220,221]. |
miR-142-3p | Up | Up | [105,136,195,200,201,222] | Attenuating | Inhibits IRI-induced cell apoptosis, autophagy, and fibrosis of the cardiomyocytes by targeting high mobility group box 1 and Rac Family Small GTPase 1 [223,224], improves cardiac function, and attenuates the myocardial inflammatory response targeting IRAK-1 [225]. |
miR-146 | Up * | Up | [91,135,136,144,182,195,200,209,226,227] | Attenuating | Protects the myocardium from IRI by inhibition of NF-kB and TRAF6/p-p38/caspase-3 signaling pathways, targeting SMAD4, EGR1, and MED1; suppresses inflammatory cytokine production via IRAK-1 and TRAF6 [228,229,230,231,232], inhibits mitochondrial dysfunction in myocardial infarction by targeting cyclophilin D [233], regulates VEGF expression in the IRI heart [234]. |
miR-150 | Up * | Up | [132,136,173,182,200] | Attenuating | Attenuates apoptosis and improves cardiac function via targeting Bax [235,236], reduces myocardial remodeling by downregulating Thioredoxin Interacting Protein [237]. |
miR-183 | Up | - | [132] | Attenuating | Reduces infarct size and attenuates apoptosis through repressing voltage-dependent anion channel 1 expression, regulation of NF-κB signaling pathway, and suppression of p27 which activates the PI3K/AKT/FOXO3a signaling pathway [238,239,240]. |
miR-486 | Up | Up | [136,174,241,242,243] | Attenuating | Inhibits apoptosis and improves cardiac function by suppressing PTEN expression, activating the PI3K/AKT signaling pathway [244,245], and targeting NDRG2 to inactivate the JNK/c-jun and NF-κB signaling pathways [246], promotes cardiac angiogenesis via fibroblastic MMP19-VEGFA cleavage signaling [247]. |
miR-29 | Up | Up * | [132,136,173,200,201] | Ambiguous | Aggravating: Increasing apoptosis and fibrosis by suppression of Mcl-2 (Bcl-2 family), IGF-1, follistatin-like 1 protein, JAK2/STAT3 pathway, and the SIRT1/AMPK/PGC1α pathway [148,149,150,151,152,248];Attenuating: Inhibition of oxidative stress, apoptosis, and promotes the viability of cardiomyocytes with IRI in vivo model via downregulation of Cyclin T2 [249]. |
miR-143 | Up | - | [136,189,195] | Ambiguous | Aggravating: Promotes cardiac ischemia-mediated mitochondrial impairment by the inhibition of protein kinase C epsilon [250], inhibits the mitosis of cardiomyocytes [251], promotes fibrosis via targeting sprouty3 [252];Attenuating: Promotes post-MI cell proliferation and reduced cell apoptosis in vitro via cyclooxygenase-2 [253] |
miR-223 | Up * | Up | [136,173,196,254,255,256] | Ambiguous | Aggravating: Increases cardiomyocyte apoptosis and oxidative stress by targeting KLF1 [257], enhances cardiac fibrosis after MI partially through targeting RASA1 [258], inhibits the angiogenesis of coronary microvascular endothelial cells in the ischemic heart [259]; Attenuating: Protects in vitro cells from hypoxia-induced apoptosis and excessive autophagy via the AKT/mTOR pathway by targeting PARP-1 [260], inhibits I/R-induced cardiac necroptosis at multiple layers [261]. |
Decreased | |||||
---|---|---|---|---|---|
miRNA | Ob | DM2 | Ref. | Effect | The Potential Regulatory Mechanism in IRI |
miR-17-5p | Down | Down | [136,189,200,201] | Aggravating | Promotes apoptosis induced by ER-stress and oxidative stress injury targeting TSG101 and STAT3 [262,263], increases apoptosis and vascular injury by suppressing the ERK pathway, and via downregulation of Bcl-2 in endothelium cells [264]. |
miR-24 | - | Down | [77,200,265] | Attenuating | Inhibits apoptosis and excessive O-GlcNAcylation [61,77]. |
miR-126 | Down | Down | [132,136,142,143,182,200,222,265] | Attenuating | Regulates oxidative stress and apoptosis via downregulation of ERRFI1 expression, and decline of PI3K/AKT pathway activity [140,141,266], decreases angiogenesis [152]. |
miR-132 | Down | - | [136,189] | Attenuating | Inhibits apoptosis and ROS production via regulation of the TUG1/miR-132-3p/HDAC3 axis and through IL-1β downregulation [267,268,269], protects against oxygen and glucose deprivation via the inhibition of FOXO3a [270], enhances neovascularization [271]. |
miR-145 | Down | Down | [136,189,272] | Attenuating | Inhibits IRI-induced apoptosis via regulation of the AKT3/mTOR and CaMKII-mediated ASK1 antiapoptotic signaling pathways, ameliorates inflammation by the NF-κB p65 pathway, and the negative regulation of CD40, protects the heart through induction of autophagy [273,274,275,276,277]; absence of miR-145 results in greater infarct thinning and dilatation [278]. |
miR-206 | Down | - | [136,279] | Attenuating | Reduces IRI-induced apoptosis, targeting protein tyrosine phosphatase 1B, Gadd45β, and ATG3 (activating PI3K/Akt/mTOR pathway); reduces infarct size and improves cardiac function [236,280,281,282]. |
miR-221 | Down | - | [104,105,136,144,194,241] | Attenuating | Reduces infarct size and prevents IRI-induced apoptosis via the PUMA/ETS-1 pathway and others [145,146]. |
miR-26a | - | Down | [142] | Ambiguous | Attenuating: Improves viability and inhibits apoptosis via regulation of the PTEN/PI3K/AKT signaling pathway, inhibition of high mobility group box 1 protein expression, inflammatory cell infiltration, and cytokine expression [156,158]. Aggravating: Possible proapoptotic mechanism via targeted regulation of the GSK3β/β-catenin signaling pathway [159] |
miR-138 | Down | - | [136,175,283] | Ambiguous | Attenuating: Reduces infarct size and myocardial I/R-induced mitochondrial apoptosis by targeting HIF-1α [284], increases the cardiac cells’ viability under hypoxia through targeting PDK1 [285]; Aggravating: Downregulation of miR-138-5p can regulate SIRT1 to inhibit cell pyroptosis and attenuate MI progression [286], miR-138 may mediate inhibition of hypoxia-induced proliferation of endothelial progenitor cells [287]. |
3.2. Smoking
3.3. Total Cholesterol Level
3.4. Systolic Blood Pressure
3.5. Physical Effort
3.6. Sex
3.7. Age
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Data Availability Statement
Conflicts of Interest
References
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Majka, M.; Kleibert, M.; Wojciechowska, M. Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury. Cells 2021, 10, 3331. https://doi.org/10.3390/cells10123331
Majka M, Kleibert M, Wojciechowska M. Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury. Cells. 2021; 10(12):3331. https://doi.org/10.3390/cells10123331
Chicago/Turabian StyleMajka, Miłosz, Marcin Kleibert, and Małgorzata Wojciechowska. 2021. "Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury" Cells 10, no. 12: 3331. https://doi.org/10.3390/cells10123331