Emerging cardioprotective mechanisms of vitamin B6: a narrative review

Kumrungsee, Thanutchaporn; Zhang, Peipei; Suda, Takafumi; Katô, Norihisa

doi:10.1007/s00394-021-02665-2

Cited by 18 publications

(13 citation statements)

References 69 publications

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“…Most patients with heart failure are short of micronutrients, of which Vitamin B deficiency is more prevalent in heart failure patients than ordinary people. Studies on the mechanism of action of riboflavin against heart failure have focused on reducing homocysteine levels, lowering chronic inflammation and suppressing oxidative stress (Kumrungsee et al, 2022). However, whether riboflavin can supply SCAD to prevent heart failure remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Riboflavin protects against heart failure via SCAD‐dependent DJ‐1–Keap1–Nrf2 signalling pathway

Cao

Zhong

et al. 2023

British J Pharmacology

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Background and PurposeOur recent studies have shown that flavin adenine dinucleotide (FAD) exerts cardiovascular protective effects by supplementing short‐chain acyl‐CoA dehydrogenase (SCAD). The current study aimed to elucidate whether riboflavin (the precursor of FAD) could improve heart failure via activating SCAD and the DJ‐1–Keap1–Nrf2 signalling pathway.Experimental ApproachRiboflavin treatment was given to the mouse transverse aortic constriction (TAC)‐induced heart failure model. Cardiac structure and function, energy metabolism and apoptosis index were assessed, and relevant signalling proteins were analysed. The mechanisms underlying the cardioprotection by riboflavin were analysed in the cell apoptosis model induced by tert‐butyl hydroperoxide (tBHP).Key ResultsIn vivo, riboflavin ameliorated myocardial fibrosis and energy metabolism, improved cardiac dysfunction and inhibited oxidative stress and cardiomyocyte apoptosis in TAC‐induced heart failure. In vitro, riboflavin ameliorated cell apoptosis in H9C2 cardiomyocytes by decreasing reactive oxygen species (ROS). At the molecular level, riboflavin significantly restored FAD content, SCAD expression and enzymatic activity, activated DJ‐1 and inhibited the Keap1–Nrf2/HO1 signalling pathway in vivo and in vitro. SCAD knockdown exaggerated the tBHP‐induced DJ‐1 decrease and Keap1–Nrf2/HO1 signalling pathway activation in H9C2 cardiomyocytes. The knockdown of SCAD abolished the anti‐apoptotic effects of riboflavin on H9C2 cardiomyocytes. DJ‐1 knockdown hindered SCAD overexpression anti‐apoptotic effects and regulation on Keap1–Nrf2/HO1 signalling pathway in H9C2 cardiomyocytes.Conclusions and ImplicationsRiboflavin exerts cardioprotective effects on heart failure by improving oxidative stress and cardiomyocyte apoptosis via FAD to stimulate SCAD and then activates the DJ‐1–Keap1–Nrf2 signalling pathway.

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Section: Discussionmentioning

confidence: 99%

Riboflavin protects against heart failure via SCAD‐dependent DJ‐1–Keap1–Nrf2 signalling pathway

Cao

Zhong

et al. 2023

British J Pharmacology

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“…Recent studies have revealed that vitamin B6 treatment increases cardiac levels of imidazole dipeptides (e.g., carnosine, anserine, and homocarnosine), histamine, and γ-aminobutyric acid and suppresses P2X7 receptor-mediated NLRP3 inflammasome. These modulations may imply potential cardioprotective mechanisms of vitamin B6 ( 33 ). Furthermore, vitamin B6 has been shown to inhibit platelet aggregation and endothelial cell proliferation, which suggests an antithrombotic effect ( 34 ).…”

Section: Discussionmentioning

confidence: 99%

Association of Plasma Vitamin B6 With Coronary Heart Disease in Patients Undergoing Diagnostic Coronary Angiography: New Insight on Sex Differences

Liu

et al. 2021

Front. Cardiovasc. Med.

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Aim: To date, findings on the overall and sex-specific effects of plasma pyridoxal 5′-phosphate (PLP, active coenzyme form of vitamin B6) on the risk of coronary heart disease (CHD) have been inconsistent. This study sought to advance our understanding on the association of plasma PLP with risk of CHD, with particular attention paid to sex differences and effect modifiers.Methods: We conducted a hospital-based, case-control study on suspected CHD patients undergoing diagnostic coronary angiography. A total of 429 CHD cases and 429 controls matched by age, sex, and operation time were included in the final analysis. Plasma PLP was assessed using LC-MS. Logistic regression analyses were performed to evaluate the association between plasma PLP and a first CHD event.Results: The mean (SD) plasma PLP levels were 8.4 (6.3) in male cases and 9.0 (11.0) in female cases, and 9.5 (8.5) in male controls and 12.5 (12.9) in female controls. Each 1 ng/mL increment in log2PLP was associated with a 28% lower risk of CHD in overall population. When stratified by sex, plasma PLP was significantly and independently associated with CHD in women (OR = 0.63, 95% CI: 0.50–0.80), but not in men (OR = 0.86, 95% CI: 0.67–1.09). The association of plasma PLP with CHD risk was modified by sex (adjusted Pinteraction = 0.022).Conclusions: We found a significant, inverse linear association between plasma PLP and CHD in Chinese women, but not in men. Our findings warrant additional investigation.

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“…There are six isoforms of B6, also known as B6 vitamers, which include pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM), and their phosphorylated forms. Among these forms, pyridoxal 5′-phosphate (PLP) is the most active and serves as a coenzyme in over 150 reactions, including the synthesis, transformation, and degradation of amino acids; the supply of one-carbon units; trans-sulfation; synthesis of tetrapyrrolic compounds, polyamines, and hydrogen sulfide (H 2 S); biosynthesis and degradation of neurotransmitters; as well as glycogen breakdown [ 1 , 2 ]. Additionally, B6 itself is known to have a radical scavenger activity [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…In Canadian young adult women, the prevalence of severe B6 deficiency (plasma PLP < 20 nmol/L) was 1.5% and that of marginal B6 deficiency (plasma PLP = 20–30 nmol/L) was 10.9% [ 4 ]. Furthermore, B6 deficiency poses a risk for heart diseases and cancers, making it an important vitamin in dietary considerations related to chronic diseases [ 1 , 2 ].…”

Section: Introductionmentioning

confidence: 99%

Relationship of Low Vitamin B6 Status with Sarcopenia, Frailty, and Mortality: A Narrative Review

Kato,

Kimoto,

Zhang

et al. 2024

Nutrients

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Marginal vitamin B6 (B6) deficiency is a widespread global concern. Inadequate B6 levels have been linked to an increased risk of age-related chronic diseases such as cardiovascular diseases and cancers. In recent years, the growing concern over sarcopenia (the age-related loss of muscle mass and strength) and frailty (a decline in physiological resilience and increased vulnerability associated with aging) is particularly relevant due to the emergence of super-aged societies in developed countries. Notably, among the thirty-one studies included in this review, twenty-five showed a significant association of B6 status with sarcopenia, frailty, and all-cause mortality in adults (p < 0.05), while six showed no association. Emerging studies have suggested novel mechanisms underlying this association. These mechanisms involve P2X7 receptor-mediated NLRP3 inflammasome signaling, AMPK signaling, PD-L1 signaling, and satellite cell-mediated myogenesis. Furthermore, the modulation of PLP-dependent enzymes due to B6 deficiency is associated with impaired metabolic processes, affecting energy utilization, imidazole peptide production, and hydrogen sulfide production, as well as the kynurenine pathway, all of which play vital roles in skeletal muscle health and pathophysiology. This narrative review provides an up-to-date assessment of our current understanding of the potential role of nutritional B6 status in combating sarcopenia, frailty, and mortality.

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Emerging cardioprotective mechanisms of vitamin B6: a narrative review

Cited by 18 publications

References 69 publications

Riboflavin protects against heart failure via SCAD‐dependent DJ‐1–Keap1–Nrf2 signalling pathway

Riboflavin protects against heart failure via SCAD‐dependent DJ‐1–Keap1–Nrf2 signalling pathway

Association of Plasma Vitamin B6 With Coronary Heart Disease in Patients Undergoing Diagnostic Coronary Angiography: New Insight on Sex Differences

Relationship of Low Vitamin B6 Status with Sarcopenia, Frailty, and Mortality: A Narrative Review

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