Table 1.
Studies reporting the effect of ROS species. The references represent the progression in the text according to those reported in the PRISMA flowchart.
| First Author/Year Ref | Type of Study | Cohort | Aims | Findings |
|---|---|---|---|---|
| Wang et al. 2017 JAHA [22] |
Rat Model | SHR WKY Control |
TRPC3 induced ROS production induced. | Improved TRPC3 activity at the cytoplasmic and mitochondrial levels. Increased redox signaling and calcium dysregulation. |
| Montezano et al. 2016 JAHA [23] |
Mice model | SM22+, Nox5+, Nox5+/SM22+ † WT |
Nox5 in pro-contractile signaling and vascular function. | Nox5 lead to join calcium and reactive oxygen species to the pro-contractile molecular apparatus in vascular smooth muscle cells. |
| Ikumi et al. 2020 J Cardiovasc Pharmacol [24] |
Mice model | eNOS-KO nNOS/eNOS-double-KO WT control |
EDH in coronary microcirculation and cardiac diastolic function. | Substantial effect of EDH/H2O2 in maintaining coronary microcirculation and cardiac diastolic function through oxidative PKGIα activation. |
| Denhartig et al. 2017 Arterioscler Thromb Vasc Biol [25] |
Mice model | C57BL/6 NOX4 deletion C57BL/6 control | NOX4-derived ROS in the development of obesity and insulin resistance. | Substantial role of NOX4-derived ROS in the onset of insulin resistance and adipose tissue inflammation. |
| Sano et al. 2017 Nutr Metab Cardiovasc Dis [26] |
Mice model | C57BL/6 HFD C57BL/6 HFD plus EC |
In vivo effects of EC on adipose tissue inflammation and obesity. | Noticable beneficial effects of EC for the prevention of adipose tissue inflammation and insulin resistance by marked suppression of CCL19. |
| Li et al. 2022 [27] PLoS One |
Rat Model | AT1aR−/− gene KO WT control |
The role of Ang II in diet-induced obesity. | AT1aR deficiency alleviated adipocyte hypertrophy in high-fat diet rats by promoting adipose lipolysis probably via cAMP/PKA pathway. |
| La Favor et al. 2016 Arterioscler Thromb Vasc Biol [28] |
Human model | Men 15 Women 27 BMI 21.6 ± 0.6 30.1 ± 0.4 36.6 ± 0.7 ℷ |
Determination the impact of in vivo ROS on microvascular endothelial function in obese human individuals. | Substantial increase activity of NADPH oxidase. Excessive ROS production in skeletal muscle of obese individuals. Association between excessive NADPH oxidase-derived ROS to microvascular endothelial dysfunction in obesity. |
| Masi et al. 2018 Arterioscler Thromb Vasc Biol [29] |
Human model | 36 obeses 31 controls |
Impact of arginase as a determinant of endothelial dysfunction in small arteries in obese individuals. | Arginase lead to microvascular endothelial dysfunction in obesity. Decreased effect of arginase in aged obese for higher levels of vascular oxidative stress. Accelerated microvascular remodeling in obese individuals. |
| Godo et al. 2016 Arterioscler Thromb Vasc Biol [30] |
Mice model | Cav-1-KO eNOS-Tg WT |
Study the probable relevance of the physiological balance between NO and EDH in cardiovascular homeostasis. | Genotypes showed altered cardiovascular phenotypes, including cardiac hypertrophy in Cav-1-KO mice and hypotension in eNOS-Tg mice. Evidence suggested that excessive endothelium-derived NO with reduced EDH impairs cardiovascular homeostasis in mice in vivo. |
| Gray et al. 2016 Arterioscler Thromb Vasc Biol [31] |
Human model Mouse model |
HAECs_ diabetic HAECs_ non diabetic |
Investigate the role of type 4 isoform (NOX4) in human and mouse atherosclerosis. | Both in humans and in mouse, the H2O2 -forming NOX4, in contrast with the superoxide-forming NOX1, can act as a negative modulator of inflammation and remodeling and convey atheroprotection. |
| Otsuka et al. 2013 Ann Cardiothorac Surg [32] |
Human model | Comparative study IMA vs. SVG |
IMA reveals fewer fenestrations, lower intercellular junction permeability. Higher antithrombotic production of heparin sulfate and tissue plasminogen activator, and NO. | IMA is the first line of defense for the treatment of coronary artery disease. |
| Freed et al. 2014 Circ Res [33] |
Human model | Human healthy adipose arterioles pretreated with ceramide | To evaluate the induction of ceramide to favor a switch from nitric oxide to H2O2. | Ceramide has an crucial role in the transition from nitric oxide to mitochondrial-derived H2O2. |
| Durand et at 2016 Arterioscler Thromb Vasc Biol [34] |
Human model | Patients with CAD | To evaluate vascular actions of angiotensin 1-7 (ANG 1-7) in human atrial and adipose arterioles. | ANG 1-7 treatment is sufficient to restore the NO component of FMD in arterioles from patients with CAD. |
| Kirsch et al. 2016 Arterioscler Thromb Vasc Biol [35] |
Mouse model | Mouse Cremaster vs. Txnrd2-deficient mice | To examine dysregulated redox homeostasis and inadequate nitric oxide signaling. | Txnrd2 plays a crucial important role in balancing mitochondrial ROS production in the endothelium. |
| Erb et al. 2016 Arterioscler Thromb Vasc Biol [36] |
Human model | Patients (n = 51) undergoing CABG with IMA | To evaluate both polymorphisms of nitric eNOS gene in the promoter (T-786C) and exon 7 (G894T). | Observed eNOS polymorphisms in larges conduits. Deteriorated endothelium-dependent vasodilatory capacity in patients with CAD. |
Abbreviations: ANG 1-7, angiotensin 1-7; Angiotensin II receptor type 1, AT1aR−/−, AT1aR gene knockout; CABG, coronary artery bypass grafting; Cav-1, caveolin-1; EC, Epicatechin; EDH, endothelium-dependent hyperpolarization; eNOS, endothelial NOS; Endothelium-derived hydrogen peroxide; H2O2; FID, flow-induced dilation; HAEC, human arterial endothelial cell; HDF, high-fat diet; IMA, internal mammary artery; KO, knockout; NADPH, nicotinamide adenine dinucleotide phosphate; NOX, NADPH oxidase; nNOS, neuronal NOS; NOS, nitric oxide synthases; PKGIα, protein kinase G I-α; ROS, reactive oxygen species; SHR, spontaneously hypertensive rat; SM, smooth muscle; Tg, transgenic; TRPC3; transient receptor potential channel, canonical type 3; WKY, wistar kyoto rat; WT, wild type; †22, protein type; ℷ obese.