The functional anomalies of the aged myocardium arise from both structural modifications and cellular and molecular changes. Heart aging is influenced by various molecular processes such as cardiac hypertrophy being a characteristic feature of this aging process in the heart (Hastings et al., 2024). As the heart ages, it undergoes hypertrophy, leading to changes in nutrient and growth signaling (Oldfield et al., 2020). The mechanistic target Rapamycin (mTOR) (Dai et al., 2023), and insulin-like growth factor-1 (IGF-1) are two significant signaling pathways that have an involvement in heart hypertrophy and aging (Abdellatif et al., 2023). The mechanistic target of rapamycin (mTOR), governs cellular development and has been shown to be a significant regulator of the aging process and age related diseases (Liu and Sabatini, 2020). Enhanced mTOR signaling hinders resilience to heart aging, whereas diminished mTOR signaling improves it in mice models (Mannick and Lamming, 2023).

In animal models, the insulin/IGF-1 signaling pathway is essential for controlling longevity. Deficiency in this signaling pathway in mice leads to a decrease in age-related dysfunction of cardiomyocytes (Lee and Kim, 2018). The decline in IGF-1 levels associated with aging increases the heart failure risk in individuals (Khan et al., 2002). The functional damage caused by dysfunctional mitochondria can shorten life expectancy by impairing cellular and organ function (Amorim et al., 2022). Age-related diseases increase mitochondrial ROS production result in enlarged, bloated, and damaged mitochondria (Liu et al., 2020; Schneider et al., 2020). In the heart, mitochondrial function is regulated by PGC-1α, also known as peroxisome proliferator-activated receptor coactivator (Qian et al., 2024).

Cardiac dysfunction results from the repression of its expression in failing hearts (He et al., 2022). Mitochondrial malfunction and aberrant ROS generation accelerate the aging process, by directly harming cellular macromolecules and interfering with normal regular signaling and energetics (Proshkina et al., 2020). The ECM, a conglomeration of proteins located outside cells, offers structural and metabolic support to neighboring cells (Karamanos et al., 2021). Cardiac fibroblasts are the main producers of ECM proteins, such as collagen, elastin, fibronectin, laminin, and fibrinogen (Halper, 2021). Heart stiffness increases when there is an abundance of ECM deposited on the heart contributed to diastolic dysfunction (Lunde et al., 2024). MMPs, TIMPs, and other proteases regulate the production and breakdown of ECM proteins (Shan et al., 2023). Aging hearts exhibit myocardial fibrosis and dysregulation of ECM protein production and breakdown. Profibrotic factors, such as transforming growth factor-β, stimulate the production of ECM proteins and hinder the breakdown of the matrix by MMPs (Antar et al., 2023; Lunde et al., 2024). The regulation of MMPs and TIMPs varies with on aging; however, their precise roles in heart aging remain inadequately understood (Rodrigues et al., 2024).

The process of heart aging causes microscopic alterations, such as an increase in the thickness of inner layer of blood vessels (intima) and the buildup of collagen. Symptoms includeelevated systolic blood pressure and pulse wave velocity, along with increase in pulse pressure (Xu et al., 2017; Liu W. et al., 2023). Left ventricular hypertrophy (LVH) may occur as a consequence of increased afterload and wall stress brought on by arterial stiffness. The volume of the myocardium remains constant with age in the heart (Đorđević et al., 2024). Research indicated that within the age range of 30–70 years, approximately 35% of the total myocytes in the ventricle are lost (Oknińska et al., 2022).

Tocounteract the loss of cells, the surviving myocytes undergo hypertrophy, accompanied by an increase in the nonmyocyte compartment. While the exact cause of cell death remains uncertain, aging is associated with a decrease in capillary density, which leads to ischemic injury, (Bradley et al., 2021). Mouse models are commonly used to study heart aging because they accurately replicate the characteristics of human heart aging (Lindsey et al., 2021). Another advantage of using mouse models to research the molecular underpinnings of heart aging is their relatively short lifespan and the availability of genetically engineered animals (García-García et al., 2021). Laboratory mice do not exhibit elevated blood pressure or adverse cholesterol and blood glucose levels, allowing researchers to study the natural heart aging process without additional cardiac complications (Badmus et al., 2023). The echocardiogram conducted on a mouse model revealed phenotypic alterations such as elevated left ventricular mass, impaired diastolic function, and deteriorated myocardial performance index (MPI), resembling the aging process of the human heart (Lazzeroni et al., 2022).

The mechanism for producing ROS is oxidative phosphorylation, which entails the transfer of electrons from NADH and FADH via four mitochondrial enzymes, culminating in the synthesis of ATP from ADP (Berthiaume et al., 2019). Electrons lost during this process generate superoxide radicals, resulting in functional degradation of tissues and damage to macromolecules. Superoxide and nitric oxide may react to form peroxynitrite, a strong oxidant that penetrates membranes and nitrates numerous enzymes. It may also be converted into hydrogen peroxide via superoxide dismutase, generating a highly reactive radical known as hydroxyl radical (Juan et al., 2021;Möller and Denicola, 2024). ROS derived from mitochondria contribute significantly to vascular dysfunction by downregulating Nrf2, decreasing NO bioavailability, and increasing the production of vasoconstrictor molecules (Pang et al., 2024). This sequence of events disrupts the mitochondrial membrane, leading to the release pro-apoptotic factors, which results in the apoptosis of plaque cells and inflammation (Chang et al., 2023).

Furthermore, ROS generated by NADPH oxidases during inflammatory reactions are essential for the endogenous production of free radicals (Banerjee et al., 2020). Individuals with a genetic deficit in NOX2 suffer chronic granulomatous disease, makingthem vulnerable to common infections (Garay et al., 2022). A baseline level of ROS is necessary for maintaining cellular homeostasis; however, excessive ROS can damage cellular macromolecules and are linked to aging and CVDs (Gianazza et al., 2021). Improved endothelial vasodilation following the inhibition of NADPH oxidase with apocynin suggests that endothelial dysfunction is mediated by NADPH oxidation (Leal et al., 2020).

Proteins including albumin, ferritin, ceruloplasmin, and transferrin regulate iron homeostasis, reduce oxidative stress, and preserve endothelial function, all of which are important in heart ageing. These proteins are mostly present in humans and animals. These do not come directly from plants, but they do include substances like iron-binding molecules, antioxidants, and phytochemicals that may affect how these proteins work. Transferrin (Tf), a monomeric glycoprotein that binds iron, is mostly synthesized in the liver. Two moles of iron in two homologous iron-binding domains may bind to 1 mole of transferrin (Talukder, 2021). It is the crucial transport protein that facilitates the movement of iron throughout the bloodstream for most vital processes (Vogt et al., 2021). Tf is internalized by cells via receptor-mediated endocytosis, whereupon it binds to the Tf receptor, functioning as a transporter to maintain intracellular iron homeostasis. Although essential for basic biological processes, iron becomes toxic in excess. Therefore, iron movement into and out of cells is prudently controlled (Leon-Sicairos et al., 2015). A system involving transferrin receptor 1, divalent metal-ion transporter 1, and other proteins carries most of the iron to cells attached to plasma transferrin (Li and Qian, 2002). Transferrin facilitates the controlled distribution of iron to cells by binding and transferring it in the bloodstream. Both an excess and a deficiency of iron may adversely affect cardiac function, making the maintenance of iron equilibrium crucial (Anderson and Vulpe, 2009). Through the Fenton reaction, unbound iron can accelerate the generation of ROS, leading to oxidative damage. Transferrin reduces the availability of free iron for the generation of ROS by sequestering it. The cornerstone of an iron-based mechanism of ischemic preconditioning that protects heart cells from iron-mediated oxidative damage associated with ischemia-reperfusion injury is the synthesis of ferritin, which is prevalent in the H subunit and sequesters redox-active iron (Talukder, 2021). A recent experiment in a mouse cardiomyocyte cell line shown that L-type channels are the principal mediators of iron absorption (Rose et al., 2011).

The importation of ferrous iron via L-type channels, leading to elevated ROS production, may hinder calcium influx, hence affecting cardiac excitation-contraction coupling, which is very sensitive to changes in cellular redox state (Cheng and Lian, 2013). This may therefore lead to suboptimal systolic and diastolic function, symptomatic of iron-overload cardiomyopathy. Recent research shown that iron accumulation mediated by the iron-binding protein Lipocalin-2 leads to cardiomyocyte apoptosis and cardiac remodeling (Xu et al., 2012). Ferritin, play key role in maintaining iron homeostasis and defending cells from iron induced oxidative stress, it is actually a primary iron storage protein (Imam et al., 2017). Ferritin plays key functions in heart aging this includes, iron regulation, cellular senescence, oxidative stress and inflammation (Rosenblum, 2023). Iron deficiency is related to reduced or impaired cardiac function, even deprived of anemia, this leads to reduced exercise capacity, as well as worse consequences in heart failure patients (Jankowska et al., 2010). While iron accumulation such as hemochromatosis, this promotes oxidative stress, fibrosis and cardiomyocyte damage (Mancardi et al., 2021). Iron deficiency is related to reduced or impaired cardiac function, even deprived of anemia, this leads to reduced exercise capacity, as well as worse consequences in heart failure patients (Kremastinos and Farmakis, 2011). While iron accumulation such as hemochromatosis, this promotes oxidative stress, fibrosis and cardiomyocyte damage (Kremastinos and Farmakis, 2011). Through impounding free iron, ferritin supports to mitigate oxidative damage, thus reducing ROS production. Though, when ferritin levels are insufficient or excess, this leads oxidative stress can accelerate heart aging (Alfei et al., 2020).

Ceruloplasmin, plays a key function in heart aging via controlling iron homeostasis and oxidative stress, it is a copper containing ferroxidase (Orzheshkovskyi and Trishchynska, 2019). In heart aging ceruloplasmin helps to mitigate ROS via oxidation of ferrous iron to ferric iron. Therefore, reducing the availability of ferric iron for Fenton reactions, which generate very toxic hydroxy radicals and thus mechanism is key to avoid iron mediated oxidative damage to cardiac tissues (Tian et al., 2022). Additionally, its antioxidant abilities contribute to the upkeep of endothelial function and the decrease of inflammation, both of which are vital for cardiac ageing (Arenas de Larriva et al., 2020). However, dysregulation of ceruloplasmin levels or role may donate to iron overload and heightened oxidative stress, henceforth deteriorating age-related heart dysfunction (Rosenblum, 2023). Numerous studies have shown that the lack of ceruloplasmin is associated with increased cardiovascular risk, underscoring its significance in preserving heart health with ageing (Fox et al., 2000; Vassiliev et al., 2005).

Albumin, plays key roles in heart aging via upholds osmatic pressure, transporting hormones and fatty acids. It is most abundant plasma protein, exerting antioxidant and anti-inflammatory effects (Shastri et al., 2024). Albumin binds and neutralizes free radicals, minimizing oxidative damage to cardiac tissues and lowering oxidative stress and inflammation in the ageing heart (Shastri et al., 2024). The ability of albumin to bind nitric oxide and promote endothelial function is essential for maintaining vascular health and treating age-related conditions including heart failure and atherosclerosis. Albumin, plays key roles in heart aging via upholds osmatic pressure, transporting hormones and fatty acids. It is most abundant plasma protein, exerting antioxidant and anti-inflammatory effects. Albumin binds and neutralizes free radicals, minimizing oxidative damage to cardiac tissues and lowering oxidative stress and inflammation in the ageing heart. The ability of albumin to bind nitric oxide and promote endothelial function is essential for maintaining vascular health and treating age-related conditions including heart failure and atherosclerosis (Belinskaia et al., 2021). Furthermore, its function in balancing and controlling fluid to minimize edema is a crucial factor in cardiac ageing, which is affected (Hankins, 2006). The decreased levels of albumin, often seen in elderly adults, have been linked with an elevated risk for cardiovascular disease, underscoring its protective role in cardiac ageing (Riviati et al., 2024).

The heart aging process is defined by key features such as progressive hypertrophy of cardiomyocytes, cardiac fibrosis, and inflammation (Hastings et al., 2024). Hypertrophied cardiomyocytes contribute to a hypoxic environment, which produces an abundance of free radicals that may damage cellular constituents (Pena et al., 2020). In response to this stress, cardiomyocytes release pro-inflammatory cytokines and chemokines, initiating an immunological response and augmenting the population of macrophages in the left ventricle (Ciutac and Dawson, 2021; Moskalik et al., 2022). Due to the poor rate of proliferation of mature cardiomyocytes, damaged areas are replaced with fibrotic scar tissue, ultimately leading to organ failure (Bishop et al., 2022). The production of ROS increases with age due to various factors, including physical, chemical, and biological agents, resulting in endothelial dysfunction and cellular damage (Scioli et al., 2020; Pacinella et al., 2022).

Furthermore, when free radicals are produced excessively or uncontrollably, they can trigger an inflammatory response, this is integral to the aging process (Sadiq, 2023). Atherosclerosis, heart problems, diabetes, and other age-related diseases are linked to persistent low-grade inflammation (Candore et al., 2010; Shen et al., 2024). The causes of this syndrome include stress and continuous antigen exposure, leading to a diminished ability to manage stressors and a gradual rise in pro-inflammatory activity (Bennett et al., 2018). The term “inflammaging” refers to the increased inflammatory response that accompanies aging, resulting in a persistent low-grade systemic pro-inflammatory condition (Giunta et al., 2022).

Aging is marked by alterations in the immune, hormonal, and adipose systems, which result in a chronic inflammatory state (Oishi and Manabe, 2016). This chronic inflammatory can lead to issues such as frailty, cognitive decline, and various cardiovascular, neurological, and vascular events (Ijaz et al., 2024). Despite its negative associations, inflammation is crucial for sustaining life and maintaining individual integrity (Ahuja et al., 2023; Baechle et al., 2023). An inflammatory state arises when pro-inflammatory compounds exceed anti-inflammatory controls (Bhol et al., 2024). The origins of this low-grade inflammatory process are still under discussion; however, one theory posits that ongoing stimulation of the immune system drives a pro-inflammatory shift (Gusev and Sarapultsev, 2024). Typically, aging leads toa gradual dysregulation of the immune response, particularly affecting cellular and adaptive immunity, with a notably impact on T cell function (Tobin et al., 2020). The persistent inflammatory condition experienced by elderly individuals is largely caused by this imbalance (Conte et al., 2022). The causes are likely multifactorial, involving chronic stimulation from viruses, bacteria, and endogenous cellular factors, along with ongoing activation of the immune system’s defenses (Endres et al., 2022).

Oral quercetin, administered at 50 mg/kg, significantly mitigates isoproterenol-induced cardiac injury by reducing pro-inflammatory mediators and enhancing anti-inflammatory and antioxidant mediators (Kumar et al., 2017). Quercetin treatment may improve heat stroke outcomes in rats by mitigating hyperthermia and cardiac damage via its anti-lipid peroxidation, antioxidant, and anti-inflammatory effects (Lin et al., 2017). The rat vena cava exhibited comparable outcomes with a reduced dosage but extended treatment duration (20 mg/kg/42 days) via the suppression of reactive oxygen species, the PI3/AKT pathway, and the release of inflammatory cytokines, possibly averting myocardial infarction and ischaemic heart disease. EGCG (40 mg/kg) mitigates myocardial damage in animals by blocking the AKT/mTOR and Hippo pathways (Ma et al., 2019), while enhancing the NQO1 antioxidant pathway (Cui et al., 2021; Huang et al., 2022; Li Y. et al., 2022).

It has been shown that the naturally occurring polyphenol molecule resveratrol, which is present in a variety of plants, may help to maintain cardiovascular health and delay the aging process (Figure 4). A wide variety of plant species, including groundnuts and grapes, contain resveratrol, a naturally occurring stilbene (Kaur et al., 2022). Future studies suggest that resveratrol could serve as a potential chemo-preventive drug due to its ability to inhibit polyphenolic cyclooxygenase. It can be isolated from red wine, grape skins and seeds, and Polygonum cuspidatum roots (Kaur et al., 2022). The cardioprotective effects caused by resveratrol are associated with a notable augmentation in antioxidant activity and mitochondrial transmembrane potential, with a decrease in oxidative damage (Yang et al., 2023a).

Curcumin, a naturally occurring substance obtained from the desiccated rhizomes of Curcuma longa L., commonly known as turmeric, is extensively used in medical practice to address an extensive range of ailments (Figure 5). Several studies have demonstrated that curcumin has positive effects on cardiac conditions and endothelial system dysfunction (Cox et al., 2022; Ghorbanzadeh et al., 2022). Research on a rat model of hypertension and ischemia have shown that curcumin may improve cardiac hemodynamic function and attenuate heart failure (Aziz et al., 2022). Additionally, by reducing OS and inflammation, it increases myocardial infarction size and boosts cardiac function after ischemia events (Hori and Nishida, 2009).

One of the most well-known dietary antioxidants is quercetin, a phenolic member of the flavonoid family that is crucial to the process of heart aging (Figure 6). It is found in vegetables, fruits, tea, wine, and many other healthy goods (Carrillo-Martinez et al., 2024). The antioxidant effects of quercetin include scavenging free radicals such superoxide, hydrogen peroxide, peroxyl, and hydroxyl (Cizmarova et al., 2023).

Epigallocatechin gallate (EGCG) is the predominant and physiologically active polyphenol found in green tea (Eng et al., 2018). As a strong redox agent, EGCG has a strong antioxidant effect and plays a significant role in heart aging (Figure 7). Its structural phenolic hydroxyl group oxidizes to produce a relatively stable molecule and serves as a hydrogen source for redox reactions. This procedure successfully rids the body of a significant amount of harmful free radicals (Singh et al., 2011).

Anthocyanins, found in vibrant fruits and vegetables, have recently been the subject of studies exploring their potential, and mechanisms in human vascular endothelial cells and rat thoracic aortas subjected to aging models (Wallace, 2011). These studies examined the ability of specific anthocyanins, such as cyanidin-3-rutinoside (C-3-R) and cyanidin-3-glucoside (C-3-G), to inhibit senescence induced by d-galactose in human endothelial cells (Lee et al., 2020). The findings demonstrated a reduction in the activity of certain markers of cellular senescence, as well as a suppression of ROS production and NADPH oxidase activity in the presence of D-galactose (Hafez et al., 2024). Anthocyanins were shown to counteract the inhibition of endothelial eNOS activity, leading to the recovery of NO levels in endothelial cells (Edirisinghe et al., 2011). It was observed that anthocyanins induced eNOS deacetylation via SIRT1, resulting in increased eNOS activity. In an in vivo study involving aged rats, administration of anthocyanin-rich mulberry extract over 8 weeks led to a reduction in oxidative stress and endothelial senescence in the aorta, as well as an increase in serum NO levels, eNOS phosphorylation, SIRT1 expression, alongside a decrease in nitro-tyrosine levels in the aorta (Lee et al., 2020).

Additionally consuming anthocyanins has been shown to enhance antioxidant defense enzymes, total antioxidant capacity, and the antioxidant properties of HDL in both preclinical and clinical populations (Garcia and Blesso, 2021). Anthocyanins exhibit direct antioxidant capabilities and indirectly stimulate Nrf2 and antioxidant gene expression, mitigating oxidative stress and inflammatory signaling in atherosclerotic plaque cells, such as macrophages and endothelial cells. This may potentially protecting against atherosclerosis and cardiovascular disease (Mohammadi N. et al., 2024).

Scientifically known as s-allyl-2-ene-1-thiosulfite, allicin is a physiologically active compound derived garlic. It demonstrates a broad spectrum of pharmacological characteristics, such as immunoregulatory, antioxidant, anti-inflammatory, renal, nerve, and cardiac protective, as well as anti-tumor effects. It has been shown that allicin and its derivatives operate biologically by modifying gene expression and interacting with a variety of signaling pathways (El-Saber Batiha et al., 2020; Gao et al., 2024). Allicin, a medication for myocardial infarction, reduces infarction area and fibrosis, increases SHP2 protein levels, and inhibits ROS in infarction tissue. However, specific knockdown of SHP2 negates ROS changes. Allicin also modulates p-PERK activation, mitigate oxidative stress in rodents (Gao et al., 2024). The study revealed that allicin exerted effects on cardiac function, myocardial fibrosis, and the modulation of NF-κB signaling pathways in the myocardial tissue of rats afflicted with diabetic cardiomyopathy. The study provided evidence that allicin exhibited positive effects on cardiac dysfunction and reduced myocardial fibrosis in the rats, possibly via facilitating the deactivation of the NF-κB signaling cascade (Ma et al., 2017).

The longevity of G. biloba L. has led to its widespread recognition as a living fossil tree. Throughout its lifespan, G. biloba L. is presumed to have acquired or evolved resistance to many diseases as a mechanism of adjusting to its surroundings. Many different phytochemicals, such as flavonoids, terpenoids, alkylphenols, and carboxylic acids, are present in the leaves of G. biloba (van Beek and Montoro, 2009; Liu X.-G. et al., 2022). Only G. biloba trees contain ginkgolides A, B, C, and J. Ginkgo contains mono-, di-, and tri-glycosides as its main flavonoids (Medicine et al., 2021). Ginkgo leaf contains several chemical compounds that have different functions, such as removing oxygen free radicals and decreasing oxidation, regulating superoxide dismutase and catalases, and removing NO. Engaging in these activities has the potential to enhance protection against heart injury and potentially reduce the likelihood of MI (Kadhim et al., 2020).

Moreover, G. biloba has the ability to stimulate the AKT signaling pathway, the activation of AKT initiates cell-specific processes, such as GSK3β phosphorylation, which protect cells from acute AMI damage and reduces the AKT signaling pathway due to cardiac ischemia-reperfusion damage (Cho et al., 2009; Lejri et al., 2019). The GBE50 is an orally given GBE formulation that corresponds to the German product, EGb761, which has been used in the treatment of AMI (Liu et al., 2013). While GBE80 activates the AKT/GSK3β/β-catenin signaling pathway, successfully preventing myocardial damage from AMI and H₂O₂-generated cardiomyocyte cytotoxicity (Zheng et al., 2021).

Additionally, the effects of GBE administration on autophagy and cardiac hypertrophy may be mitigated by the SIRT1 inhibitor EX-527, which also lowers Ang II oxidative stress and the production of SIRT1 and FoxO1. This implies that GBE may be useful as a medication to treat pathological heart hypertrophy (Jiang et al., 2021). GBE has demonstrated cardioprotective properties in individuals with diabetes, namely, in the context of DCM. Investigation demonstrates that giving diabetic rats GBE treatment successfully lowers metabolic irregularities, enhances cardiac function, and lessens degenerative changes to the heart. GBE treatment, however, may be able to address defective autophagy and dysregulation of the AMPK/mTOR signaling pathway. GBE demonstrated a reduction in apoptosis produced by HG in H9C2 cells in vitro (Yang et al., 2023b). The study establishes a correlation between heightened cardiac oxidative stress, inflammation, apoptosis, and histo-morphological alterations in cardiotoxicity generated by Cs-A.

Furthermore, GBE administration has been shown to reduce the cardiotoxic effects of Cs-A by activating the mTOR/ERK1/2 signaling pathways. The aforementioned pathways are linked to the suppression of oxidative stress and inflammatory mechanisms, thereby serving as a preventive measure against heart injury. Immunohistochemistry and bio-chemical assays were employed in the study to demonstrate that the supplementation of GBE leads to a reduction in cardiotoxicity through the enhancement of the mTOR/ERK1/2 signaling pathways (Asiwe et al., 2024). The extract of GBE shown significant efficacy in mitigating myocardial infarction through the enhancement of the body’s inherent antioxidant defense mechanism and the reduction of inflammatory cytokine release and heart injury marker enzymes. The leaves of GBE, specifically EGb761, are commonly used to treat cerebrovascular diseases due to their neuroprotective proper-ties. Studies have demonstrated the protective effect of EGb761 on rats’ cognitive performance, involves preventing apoptosis and autophagy in models of VD, as well as improving cognitive performance in rats with VD through the activation of AMPK-mTOR signaling (Yin et al., 2024).

Berberine (BBR), a fundamental constituent of the Chinese herb Rhizoma coptidis, is an iso-quinoline alkaloid derived from Berberidaceae (Phogat et al., 2024). Recent research has shown that BBR possess strong anti-dysenteric qualities in addition to a variety of cardiovascular pharmacological actions, such as controlling dyslipidemia, preventing arrhythmias, inhibiting heart failure, myocardial remodeling, and lowering blood pressure. BBR prevents cardiac senescence by boosting cardiac myocytes production of KL mRNA and protein and controlling the KL/SIRT1 signaling pathway, thereby enhancing its protective effects (Li C. et al., 2022). BBR has the ability to improve diabetic cardiomyopathy by increasing the expression of myocardial methionine sulfoxide reductase A (MsrA) and simultaneously inhibiting cardiac CaMKII oxidation (Sun et al., 2023). It has been investigated by Wang et al., 2023, that BBR and its derivative tetrahydroberberrubine (THBru) improve cardiac remodeling and reduce heart aging. Compared to BBR, THBru has a greater anti-heart aging effect because it prevents heart aging via PHB2-mediated mitophagy (Wang L. et al., 2023).

Moreover, researchers are progressively focused on investigating the impact of plant-derived antioxidant on heart aging. This has led to an exploration of various chemical compounds produced from plants, with the aim of promoting cardiovascular health and mitigating the adverse effects of aging on the heart. An excellent proof is seen in several naturally occurring compounds present in plants. These drugs have garnered considerable interest owing to their potential advantages for cardiovascular health, such as enhancing endothelial function, reducing inflammation, and demonstrating antioxidant qualities (Table 1). The effects outlined above are particularly relevant to the phenomenon of heart aging, as they have the potential to mitigate the oxidative stress and inflammation associated with the aging of the cardiovascular system. The research findings indicate that these antioxidants may aid in preserving optimal heart function and vascular health, perhaps decelerating the heart aging process.