Recent Progress in Environmental Toxins-Induced Cardiotoxicity and Protective Potential of Natural Products

Yang, Youliang; Wei, Shanshan; Zhang, Bikui; Li, Wenqun

doi:10.3389/fphar.2021.699193

Cited by 11 publications

(13 citation statements)

References 139 publications

(151 reference statements)

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“…An example is a fungus-derived fingolimod drug, which the FDA approved for the treatment of multiple sclerosis [ 345 , 346 ]. One of the major advantages of NPs in drug discovery is that they confer multiple “targets” by targeting more than one signaling pathway [ 347 ]. In addition, most NPs showed beneficial effects through their antioxidant, anti-inflammatory, and anti-apoptotic properties.…”

Section: Discussionmentioning

confidence: 99%

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

et al. 2022

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Bisphenol A (BPA) is a ubiquitous environmental toxin with deleterious endocrine-disrupting effects. It is widely used in producing epoxy resins, polycarbonate plastics, and polyvinyl chloride plastics. Human beings are regularly exposed to BPA through inhalation, ingestion, and topical absorption routes. The prevalence of BPA exposure has considerably increased over the past decades. Previous research studies have found a plethora of evidence of BPA’s harmful effects. Interestingly, even at a lower concentration, this industrial product was found to be harmful at cellular and tissue levels, affecting various body functions. A noble and possible treatment could be made plausible by using natural products (NPs). In this review, we highlight existing experimental evidence of NPs against BPA exposure-induced adverse effects, which involve the body’s reproductive, neurological, hepatic, renal, cardiovascular, and endocrine systems. The review also focuses on the targeted signaling pathways of NPs involved in BPA-induced toxicity. Although potential molecular mechanisms underlying BPA-induced toxicity have been investigated, there is currently no specific targeted treatment for BPA-induced toxicity. Hence, natural products could be considered for future therapeutic use against adverse and harmful effects of BPA exposure.

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Section: Discussionmentioning

confidence: 99%

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

et al. 2022

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“…While the mechanisms of drug toxicity are heavily studied in animal hearts, the real effect and mechanisms in human cardiomyocytes are less well understood [ 36 ], which prompted the development of HTS for mitochondrial toxicants in human-relevant platforms. In addition to drug-induced mitochondrial toxicity, accumulating studies have pointed out that environmental toxins, including various pesticides and heavy metals, may also induce cardiotoxicity [ 401 , 402 ]. Hence, HTS may be useful in applications beyond the regular drug discovery pipeline.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation

Tang

Wang

et al. 2022

Pharmaceutics

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Drug-induced cardiotoxicity not only leads to the attrition of drugs during development, but also contributes to the high morbidity and mortality rates of cardiovascular diseases. Comprehensive testing for proarrhythmic risks of drugs has been applied in preclinical cardiac safety assessment for over 15 years. However, other mechanisms of cardiac toxicity have not received such attention. Of them, mitochondrial impairment is a common form of cardiotoxicity and is known to account for over half of cardiovascular adverse-event-related black box warnings imposed by the U.S. Food and Drug Administration. Although it has been studied in great depth, mitochondrial toxicity assessment has not yet been incorporated into routine safety tests for cardiotoxicity at the preclinical stage. This review discusses the main characteristics of mitochondria in cardiomyocytes, drug-induced mitochondrial toxicities, and high-throughput screening strategies for cardiomyocytes, as well as their proposed integration into preclinical safety pharmacology. We emphasize the advantages of using adult human primary cardiomyocytes for the evaluation of mitochondrial morphology and function, and the need for a novel cardiac safety testing platform integrating mitochondrial toxicity and proarrhythmic risk assessments in cardiac safety evaluation.

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“…Fetuin-A has been proposed as an endogenous inhibitor of pathological mineralization or calcification. [22][23][24] An essential role for fetuin-A in attenuating injury and infection-elicited inflammatory responses has been well described. 25,26 Studies have shown that fetuin-A at high concentration remarkably inhibits endotoxin-induced release of proinflammatory mediators, that is, TNF, IL-1, and nitric oxide in macrophage cultures, signifying anti-inflammatory potential of fetuin-A.…”

Section: Introductionmentioning

confidence: 99%

“…The intense release of inflammatory mediators elicits the generation of reactive oxygen species and causes tissue damage 22 . In sepsis‐induced cardiotoxicity, the cardiomyocyte oxidative stress reaction has been considered a hallmark and further trigger of endogenous antioxidant activity, as well as exogenous administration of antioxidant agents, has been shown to confer significant cardioprotection 23 . Therefore, attenuating inflammation and oxidative stress along with improvement in myocardial injury is considered the best potential therapeutic strategy for sepsis‐induced cardiomyopathy.…”

Section: Introductionmentioning

confidence: 99%

Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

Hassan

Hanifa

Navik

et al. 2023

Fundamemntal Clinical Pharma

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Sepsis‐induced myocardial injury is a consequence of septicemia and is one of the major causes of death in intensive care units. A serum glycoprotein called fetuin‐A is secreted largely by the liver, tongue, placenta, and adipose tissue. Fetuin‐A has a variety of biological and pharmacological properties. The anti‐inflammatory and antioxidant glycoprotein fetuin‐A has shown its efficacy in a number of inflammatory disorders including sepsis. However, its protective role against sepsis‐induced myocardial injury remains elusive. The purpose of this work is to explore the role of fetuin‐A in mouse models of myocardial injury brought on by cecal ligation and puncture (CLP). CLP significantly induced the myocardial injury assessed in terms of elevated myocardial markers (serum CK‐MB, cTnI levels), inflammatory markers (IL‐6, TNF‐α) in the serum, and oxidative stress markers (increased MDA levels and decreased reduced glutathione) in heart tissue homogenate following 24 h of ligation and puncture. Further, hematoxylin and eosin (H&E) staining showed considerable histological alterations in the myocardial tissue of sepsis‐developed mice. Interestingly, fetuin‐A pretreatment (50 and 100 mg/kg) for 4 days before the CLP procedure significantly improved the myocardial injury and was evaluated in perspective of a reduction in the CK‐MB, cTnI levels, IL‐6, and TNF‐α in sepsis‐developed animals. Fetuin‐A pretreatment significantly attenuated the oxidative stress and improved the myocardial morphology in a dose‐dependent manner. The present study provides preliminary evidence that fetuin‐A exerts protection against sepsis‐induced cardiac dysfunction in vivo via suppression of inflammation and oxidative damage.

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Recent Progress in Environmental Toxins-Induced Cardiotoxicity and Protective Potential of Natural Products

Cited by 11 publications

References 139 publications

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

Natural Products in Mitigation of Bisphenol A Toxicity: Future Therapeutic Use

Assessing Drug-Induced Mitochondrial Toxicity in Cardiomyocytes: Implications for Preclinical Cardiac Safety Evaluation

Exogenous fetuin‐A protects against sepsis‐induced myocardial injury by inhibiting oxidative stress and inflammation in mice

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