Erratum to: Multidisciplinary approach and anesthetic management of a surgical cancer patient with methylene tetrahydrofolate reductase deficiency: a case report and review of the literature

Cascella, Marco; Arcamone, Manuela; Morelli, Emanuela; Viscardi, Daniela; Russo, V.; Franciscis, Silvia De; Belli, Andrea; Accardo, Rosanna; Caliendo, Domenico; Luca, Elena De; Caprio, Barbara Di; Sauro, Francesca; Giannoni, Giovanni; Iermano, Carmine; Maciariello, Maria M M; Marracino, M.; Cuomo, Arturo

doi:10.1186/s13256-015-0706-5

Cited by 11 publications

(11 citation statements)

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“…Homocysteine (Hcy) has been studied extensively for over 30 years for its unique involvement in an increasing number of human diseases (Hankey and Eikelboom 1999;Narayanan et al 2014;Stipanuk and Ueki 2011). The Hcy level is controlled by two major processes: around 50% of Hcy enters the transsulfuration pathway to produce cysteine, and the other half is remethylated back to methionine (Met) via the folate 1-carbon cycle (Cascella et al 2015;Veeranki and Tyagi 2013). Hcy is generally present in blood in four different forms: approximately 1% as free thiol, 70-80% as a disulfide-bound to plasma proteins and the remaining 20-30% as a homodimer or heterodimer with other thiols (Hankey and Eikelboom 1999).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide improves postischemic neoangiogenesis in the hind limb of cystathionine-β-synthase mutant mice via PPAR-γ/VEGF axis

et al. 2018

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Neoangiogenesis is a fundamental process which helps to meet energy requirements, tissue growth, and wound healing. Although previous studies showed that Peroxisome proliferator‐activated receptor (PPAR‐γ) regulates neoangiogenesis via upregulation of vascular endothelial growth factor (VEGF), and both VEGF and PPAR‐γ expressions were inhibited during hyperhomocysteinemic (HHcy), whether these two processes could trigger pathological effects in skeletal muscle via compromising neoangiogenesis has not been studied yet. Unfortunately, there are no treatment options available to date for ameliorating HHcy‐mediated neoangiogenic defects. Hydrogen sulfide (H2S) is a novel gasotransmitter that can induce PPAR‐γ levels. However, patients with cystathionine‐β‐synthase (CBS) mutation(s) cannot produce a sufficient amount of H2S. We hypothesized that exogenous supplementation of H2S might improve HHcy‐mediated poor neoangiogenesis via the PPAR‐γ/VEGF axis. To examine this, we created a hind limb femoral artery ligation (FAL) in CBS +/− mouse model and treated them with GYY4137 (a long‐acting H2S donor compound) for 21 days. To evaluate neoangiogenesis, we used barium sulfate angiography and laser Doppler blood flow measurements in the ischemic hind limbs of experimental mice post‐FAL to assess blood flow. Proteins and mRNAs levels were studied by Western blots and qPCR analyses. HIF1‐α, VEGF, PPAR‐γ and p‐eNOS expressions were attenuated in skeletal muscle of CBS +/− mice after 21 days of FAL in comparison to wild‐type (WT) mice, that were improved via GYY4137 treatment. We also found that the collateral vessel density and blood flow were significantly reduced in post‐FAL CBS +/− mice compared to WT mice and these effects were ameliorated by GYY4137. Moreover, we found that plasma nitrite levels were decreased in post‐FAL CBS +/− mice compared to WT mice, which were mitigated by GYY4137 supplementation. These results suggest that HHcy can inhibit neoangiogenesis via antagonizing the angiogenic signal pathways encompassing PPAR‐γ/VEGF axis and that GYY4137 could serve as a potential therapeutic to alleviate the harmful metabolic effects of HHcy conditions.

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Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide improves postischemic neoangiogenesis in the hind limb of cystathionine-β-synthase mutant mice via PPAR-γ/VEGF axis

et al. 2018

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“…After generation of Hcy by MET-cycle, around 50% goes to the transsulfuration pathway for production of glutathione (an antioxidant), and the rest is re-methylated back to MET via the folate cycle (Fig. 1) (Cascella et al 2015; Stipanuk and Ueki 2011; Veeranki and Tyagi 2013).…”

Section: Metabolism Of Homocysteine and Hyperhomocysteinemiamentioning

confidence: 99%

“…Homocysteine (Hcy) has been studied extensively for over 30 years for its unique involvement in an increasing number of human diseases (Hankey and Eikelboom 1999; Narayanan et al 2014; Stipanuk and Ueki 2011). It is generated via methionine cycle (MET-cycle), and its level is controlled by 2 processes: around 50% of Hcy goes to transsulfuration pathway to produce cysteine and the remaining 50% is re-methylated back to methionine (MET) via folate cycle (Cascella et al 2015; Majumder et al 2017; Veeranki and Tyagi 2013). Normal total plasma Hcy concentration in our body is 5–10 μmol/L, however in a diseased condition, i.e., in hyperhomocysteinemia (HHcy), total plasma Hcy levels increases (>15 μmol/L) (Lehotský et al 2016).…”

Section: Introductionmentioning

confidence: 99%

Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress condition

Majumder

Singh

George

et al. 2019

Can. J. Physiol. Pharmacol.

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Elevated homocysteine (Hcy), i.e., hyperhomocysteinemia (HHcy), causes skeletal muscle myopathy. Among many cellular and metabolic alterations caused by HHcy, oxidative and endoplasmic reticulum (ER) stress are considered the major ones; however, the precise molecular mechanism(s) in this process is unclear. Nevertheless, there is no treatment option available to treat HHcy-mediated muscle injury. Hydrogen sulfide (H2S) is increasingly recognized as a potent anti-oxidant, anti-apoptotic/necrotic/pyroptotic, and anti-inflammatory compound and also has been shown to improve angiogenesis during ischemic injury. Patients with CBS mutation produce less H2S, making them vulnerable to Hcy-mediated cellular damage. Many studies have reported bidirectional regulation of ER stress in apoptosis through JNK activation and concomitant attenuation of cell proliferation and protein synthesis via PI3K/AKT axis. Whether H2S mitigates these detrimental effects of HHcy on muscle remains unexplored. In this review, we discuss molecular mechanisms of HHcy-mediated oxidative/ER stress responses, apoptosis, angiogenesis, and atrophic changes in skeletal muscle and how H2S can restore skeletal muscle homeostasis during HHcy condition. This review also highlights the molecular mechanisms on how H2S could be developed as a clinically relevant therapeutic option for chronic conditions that are aggravated by HHcy.

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“…Hcy in the blood is generally present in 4 different forms: (1) around 1% as free thiol, (2) 70%-80% as a disulfide-bound to plasma proteins and remaining (3) 20%-30% as a homodimer with itself, or (4) heterodimer with other thiols (Hankey and Eikelboom 1999). Levels of the Hcy are usually controlled by 2 biochemical processes: (1) roughly ϳ50% of the Hcy goes to transsulfuration pathway for producing the glutathione and the remaining (2) ϳ50% can be remethylated back to methionine (Cascella et al 2015;Veeranki and Tyagi 2013). Normally, the synthesis and elimination of Hcy stay pretty much in balance, but in diseased conditions, i.e., in HHcy, the overall plasma Hcy levels tend to increase due to the errors in the Hcy metabolism (Hamelet et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Genes and genetics in hyperhomocysteinemia and the “1-carbon metabolism”: implications for retinal structure and eye functions

George

Majumder

Ice

et al. 2020

Can. J. Physiol. Pharmacol.

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Homocysteine (Hcy), a sulfur-containing nonproteinogenic amino acid, is generated as a metabolic intermediate. Hcy constitutes an important part of the “1-carbon metabolism” during methionine turnover. Elevated levels of Hcy known as hyperhomocysteinemia (HHcy) results from vitamin B deficiency, lack of exercise, smoking, excessive alcohol intake, high-fat and methionine-rich diet, and the underlying genetic defects. These factors directly affect the “1-carbon metabolism (methionine–Hcy–folate)” of a given cell. In fact, the Hcy levels are determined primarily by dietary intake, vitamin status, and the genetic blueprint of the susceptible individual. Although Hcy performs an important role in cellular functions, genetic alterations in any of the key enzymes responsible for the “1-carbon metabolism” could potentially upset the metabolic cycle, thus causing HHcy environment in susceptible people. As such, HHcy relates to several clinical conditions like atherosclerosis, myocardial infarction, stroke, cognitive impairment, dementia, Parkinson’s disease, multiple sclerosis, epilepsy, and ocular disorders, among others. This article summarizes the findings from our laboratory and public database regarding genetics of HHcy and its effects on ocular disorders, their respective management during dysregulation of the 1-carbon metabolism.

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Erratum to: Multidisciplinary approach and anesthetic management of a surgical cancer patient with methylene tetrahydrofolate reductase deficiency: a case report and review of the literature

Cited by 11 publications

References 1 publication

Hydrogen sulfide improves postischemic neoangiogenesis in the hind limb of cystathionine-β-synthase mutant mice via PPAR-γ/VEGF axis

Hydrogen sulfide improves postischemic neoangiogenesis in the hind limb of cystathionine-β-synthase mutant mice via PPAR-γ/VEGF axis

Restoration of skeletal muscle homeostasis by hydrogen sulfide during hyperhomocysteinemia-mediated oxidative/ER stress condition

Genes and genetics in hyperhomocysteinemia and the “1-carbon metabolism”: implications for retinal structure and eye functions

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