Fucoxanthin alleviates myocardial fibrosis in diabetic mice by suppressing oxidative stress in cardiac fibroblasts via Prdx4 regulation

Q: What are the key findings of this study?

Fucoxanthin increased the 12-week survival rate from 50% to 80% and alleviated myocardial fibrosis in mice with diabetic cardiomyopathy by upregulating Prdx4.

Q: What is the clinical evidence from this study?

Population: Diabetic cardiomyopathy (n=32). Intervention: Fucoxanthin vs. Sodium citrate buffer (Control) or untreated DCM. Primary outcome: Survival rate at 12 weeks (p=<0.05).

Q: What does this research mean for the field?

Fucoxanthin alleviates myocardial fibrosis and cardiac dysfunction in diabetic cardiomyopathy by suppressing oxidative stress and proliferation in cardiac fibroblasts through the upregulation of Prdx4. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To determine whether fucoxanthin attenuates myocardial fibrosis in diabetic cardiomyopathy and to identify the mediating role of peroxiredoxin 4 in suppressing cardiac fibroblast oxidative stress.

Huiying Sun; Mingyu Li; Xiaowan Zhao; Liuxing Wang; Yebei Liu; Yangyang Gao; Y S Wang; Chao Yang; Jianwen Zhou; Hongxia Cui; Xuemei Zhao; Cuiyan Han; Juan Song; Qi Zhang

doi:10.1038/s41598-026-69072-7

September 11, 2026Scientific ReportsOpen Access

Fucoxanthin alleviates myocardial fibrosis in diabetic mice by suppressing oxidative stress in cardiac fibroblasts via Prdx4 regulation

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Key result

Fucoxanthin cuts mortality ~60% and alleviates fibrosis in mice with diabetic cardiomyopathy via Prdx4.

P<0.05
n=32

Why the study?

Cardiac fibrosis is a serious pathological manifestation of diabetic cardiomyopathy that damages cardiac function and leads to heart failure, necessitating effective treatments.

Does fucoxanthin improve cardiac dysfunction and myocardial fibrosis in a mouse model of diabetic cardiomyopathy?

Key Points

To determine whether fucoxanthin attenuates myocardial fibrosis in diabetic cardiomyopathy and to identify the mediating role of peroxiredoxin 4 in suppressing cardiac fibroblast oxidative stress.
Diabetic cardiomyopathy was induced in mice using intraperitoneal streptozotocin at 50 mg/kg per day for 5 consecutive days, followed by 12 weeks of observation with or without fucoxanthin treatment (n=10 per group for survival).
Primary cardiac fibroblasts were cultured under high-glucose conditions, treated with fucoxanthin, and subjected to siRNA-mediated knockdown of Prdx4 to evaluate cell proliferation, transformation, and oxidative stress.
In diabetic mice, fucoxanthin increased 12-week survival from 50 to 80% (P < 0.05 vs. DCM), prevented declines in ejection fraction and fractional shortening, and suppressed myocardial interstitial collagen deposition alongside Col1 and Col3 expression.
In cardiac fibroblasts exposed to high glucose, fucoxanthin reduced reactive oxygen species, restored mitochondrial membrane potential, and suppressed α-SMA, Col1, and Col3 expression (P < 0.05 vs. HG).
Silencing Prdx4 abrogated the protective effects of fucoxanthin, increasing intracellular reactive oxygen species, cell proliferation, and collagen expression in high-glucose conditions.

Structured PICO

Does fucoxanthin improve cardiac dysfunction and myocardial fibrosis in a mouse model of diabetic cardiomyopathy?

P

Population

32 8-week-old male mice with streptozotocin-induced diabetic cardiomyopathy, treated with fucoxanthin and followed for 12 weeks.

I

Intervention

Fucoxanthin (FX) 50 mg/kg/day via gavage for 4 weeks (in vivo); FX 5 μmol/L for 48 hours (in vitro).

C

Comparator

Control mice receiving sodium citrate buffer and diabetic cardiomyopathy mice receiving no fucoxanthin (in vivo); normal glucose and high glucose media without fucoxanthin (in vitro).

O

Outcome

Cardiac dysfunction (ejection fraction, fractional shortening) and myocardial fibrosis (collagen deposition, Col1 and Col3 expression).surrogate

Main Result

Absolute Event Rate: 80% vs 50%

Absolute Risk Reduction: 30%

p-value: p=<0.05

Fucoxanthin alleviates diabetic myocardial fibrosis and cardiac dysfunction in mice by suppressing oxidative stress via Prdx4 upregulation.

Limitations

Animal experiments were conducted exclusively in STZ-induced type 1 diabetic mice, so effects in type 2 diabetes are unknown.
Mechanistic validation was performed primarily in cultured cardiac fibroblasts without in vivo confirmation of the Prdx4-dependent pathway.
The data do not distinguish between direct and indirect regulation of Prdx4 by FX.
The molecular mechanisms by which FX upregulates Prdx4 remain unclear.

Implication

Should not yet alter diabetic cardiomyopathy management; hypothesis-generating for fucoxanthin in cardiac fibrosis models.

Abstract

Cardiac fibrosis is a serious pathological manifestation of diabetic cardiomyopathy (DCM), which can damage cardiac function and eventually lead to heart failure. This study demonstrated that fucoxanthin (FX), the most abundant carotenoid in the marine environment, significantly ameliorated cardiac dysfunction and reduced fibrosis levels in mice with DCM. FX was found to decrease the expression levels of both collagen type I (Col1) and collagen type III (Col3), which are key markers of fibrosis. Additionally, in vitro experiments further revealed that FX potently inhibited the proliferation and transformation of cardiac fibroblasts, accompanied by a notable downregulation of Col1 and Col3 expression. Furthermore, our results indicated that FX elevated mitochondrial membrane potential and decreased reactive oxygen species (ROS) levels in cardiac fibroblasts exposed to high glucose (HG) conditions. At the mechanistic level, FX was observed to markedly upregulate the expression of the antioxidant protein peroxiredoxin 4 (Prdx4) in these cells. Silencing of Prdx4 attenuated the suppressive effects of FX on both proliferation and oxidative stress in cardiac fibroblasts. In summary, FX mitigates HG-induced oxidative stress, cellular proliferation, and transformation within cardiac fibroblasts, with Prdx4 playing a critical role in mediating these effects, ultimately contributing to the alleviation of diabetic myocardial fibrosis. These findings demonstrate the pivotal role of FX in the prevention and treatment of myocardial fibrosis in diabetic mice, and have characterized Prdx4 as a crucial mediator in the FX-induced prevention of myocardial fibrosis in mice with DCM.

Discussion

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Cite This Study

Sun et al. (2026) studied Diabetic cardiomyopathy (n=32). Fucoxanthin vs. Sodium citrate buffer (Control) or untreated DCM was evaluated on Survival rate at 12 weeks (p=<0.05). Fucoxanthin increased the 12-week survival rate from 50% to 80% and alleviated myocardial fibrosis in mice with diabetic cardiomyopathy by upregulating Prdx4.

synapsesocial.com/papers/6aa7afef79e9260bc85aacc5 https://doi.org/10.1038/s41598-026-69072-7

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Fucoxanthin alleviates myocardial fibrosis in diabetic mice by suppressing oxidative stress in cardiac fibroblasts via Prdx4 regulation

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

Fucoxanthin alleviates myocardial fibrosis in diabetic mice by suppressing oxidative stress in cardiac fibroblasts via Prdx4 regulation

Key Points

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Cite This Study

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