Basic Science and Pathogenesis.

Background: Our previous studies reported that D-galactose (D-gal) administration for four to eight weeks caused metabolic disturbance, brain mitochondrial dysfunction, and brain aging, leading to cognitive dysfunction in similar with natural aging condition. Spermidine is a polyamine that can be found naturally. Spermidine has been showed the beneficial effects on various models, such as attenuating metabolic/gut impairments in obesity, and ameliorating memory loss in aged model.

Basic Science and Pathogenesis.

Background: An increase in the development of learning deficit occurred during estrogen-deprived periods via the increment of systemic and brain oxidative stress, brain apoptosis, and synaptic dysplasticity. Although estrogen supplementation has been shown to improve the brain function in estrogen-deprived conditions, it can lead to several adverse effects. Therefore, the novel therapeutic approach with minimal side effects to protect brain function in estrogen-deprived conditions should be further investigated.

Basic Science and Pathogenesis.

Background: Sodium glucose transporter 2 inhibitor (SGLT2i) is the latest guideline-directed medical therapy for patients with heart failure, as it has demonstrated favorable cardiovascular outcomes in heart failure (HF) patients with or without diabetes. Furthermore, SGLT2i has effectively improved cognitive function in older adults with diabetes and HF. However, the effects of SGLT2i on cognitive function and brain mitochondrial function in rats with ischemic HF have never been investigated.

Microalgae-fungal pellets as novel dual-bioadsorbents for dye and their practical applications in bioremediation of palm oil mill effluent.

Microalgae-fungal pellets were applied as novel dual-biosorbents for dye removal compared to fungal pellets. Both pellet types effectively removed anionic dyes better than cationic dyes, with the maximum adsorbing efficiency being nearly 100 % at a wide pH range of 3-8. The adsorption isotherms of anionic Congo Red dye and Coomassie brilliant blue R-250 dye using both pellet types and their biosorption kinetics were intensively studied.

Microalgae growth-promoting bacteria for cultivation strategies: Recent updates and progress.

Microalgae growth-promoting bacteria (MGPB), both actinobacteria and non-actinobacteria, have received considerable attention recently because of their potential to develop microalgae-bacteria co-culture strategies for improved efficiency and sustainability of the water-energy-environment nexus. Owing to their diverse metabolic pathways and ability to adapt to diverse conditions, microalgal-MGPB co-cultures could be promising biological systems under uncertain environmental and nutrient conditions. This review proposes the recent updates and progress on MGPB for microalgae cultivation through co-culture strategies.

Chronic mitochondrial dynamic-targeted therapy alleviates left ventricular dysfunction by reducing multiple programmed cell death in post-myocardial infarction rats.

Mitochondrial dysfunction and the activation of multiple programmed cell death (PCD) have been shown to aggravate the severity and mortality associated with the progression of myocardial infarction (MI). Although pharmacological modulation of mitochondrial dynamics, including treatment with the fusion promoter (M1) and the fission inhibitor (Mdivi-1), exerted cardioprotection against several cardiac complications, their roles in the post-MI model have never been investigated. Using a MI rat model instigated by permanent left-anterior descending (LAD) coronary artery occlusion, post-MI rats were randomly assigned to receive one of 4 treatments (n = 10/group): vehicle (DMSO 3%V/V), enalapril (10 mg/kg), Mdivi-1 (1.

Donepezil ameliorates gut barrier disruption in doxorubicin-treated rats.

An impact of donepezil against doxorubicin-induced gut barrier disruption and gut dysbiosis has never been investigated. Twenty-four male Wistar rats were divided into three groups. Each group was treated with either vehicle as a control, doxorubicin, or doxorubicin-cotreated with donepezil.

Future perspectives on the roles of mitochondrial dynamics in the heart in obesity and aging.

Increasing global obesity rates and an aging population are independently linked to cardiac complications. Consequently, it is crucial to comprehensively understand the mechanisms behind these conditions to advance innovative therapies for age-related diseases. Mitochondrial dysfunction, specifically defects in mitochondrial fission/fusion processes, has emerged as a central regulator of cardiac complications in aging and age-related diseases (e.

Modulating Mitochondrial Dynamics Mitigates Cognitive Impairment in Rats with Myocardial Infarction.

Background: We have previously demonstrated that oxidative stress and brain mitochondrial dysfunction are key mediators of brain pathology during myocardial infarction (MI).

Objective: To investigate the beneficial effects of mitochondrial dynamic modulators, including mitochondrial fission inhibitor (Mdivi-1) and mitochondrial fusion promotor (M1), on cognitive function and molecular signaling in the brain of MI rats in comparison with the effect of enalapril.

Methods: Male rats were assigned to either sham or MI operation.

Ferroptosis inhibitor improves cardiac function more effectively than inhibitors of apoptosis and necroptosis through cardiac mitochondrial protection in rats with iron-overloaded cardiomyopathy.

Iron overload cardiomyopathy (IOC) is the leading cause of death in cases of iron overload in patients. Previous studies demonstrated that iron overload led to cardiomyocyte dysfunction and death through multiple pathways including apoptosis, necroptosis and ferroptosis. However, the dominant cell death pathway in the iron-overloaded heart needs clarification.

Vagus nerve stimulation and acetylcholinesterase inhibitor donepezil provide cardioprotection against trastuzumab-induced cardiotoxicity in rats by attenuating mitochondrial dysfunction.

Trastuzumab (Trz) is a targeted anticancer drug for human epidermal growth factor receptor 2 (HER2)-positive tumors, as Trz-induced cardiotoxicity (TIC) is commonly observed in Trz-treated patients. Since cardiac autonomic modulation with electrical vagus nerve stimulation (VNS) and acetylcholinesterase (AChE) inhibitors exerts cardioprotection against various heart diseases, the comparative effects of electrical VNS and an AChE inhibitor (donepezil) on cardiac and mitochondrial functions and programmed cell death pathways in TIC are not known. VNS devices were implanted in thirty-two male Wistar rats and were divided into 4 groups: (i) Control-Sham (CSham), (ii) Trz-Sham (TSham), (iii) Trz-VNS (TVNS), and (iv) Trz-donepezil (TDPZ).

Acetylcholinesterase inhibition protects against trastuzumab-induced cardiotoxicity through reducing multiple programmed cell death pathways.

Background: Trastuzumab (Trz)-induced cardiotoxicity (TIC) is one of the most common adverse effects of targeted anticancer agents. Although oxidative stress, inflammation, mitochondrial dysfunction, apoptosis, and ferroptosis have been identified as potential mechanisms underlying TIC, the roles of pyroptosis and necroptosis under TIC have never been investigated. It has been shown that inhibition of acetylcholinesterase function by using donepezil exerts protective effects in various heart diseases.

Microalgae as tools for bio-circular-green economy: Zero-waste approaches for sustainable production and biorefineries of microalgal biomass.

Microalgae are promising organisms that are rapidly gaining much attention due to their numerous advantages and applications, especially in biorefineries for various bioenergy and biochemicals. This review focuses on the microalgae contributions to Bio-Circular-Green (BCG) economy, in which zero-waste approaches for sustainable production and biorefineries of microalgal biomass are introduced and their possible integration is discussed. Firstly, overviews of wastewater upcycling and greenhouse gas capture by microalgae are given.

Differential temporal therapies with pharmacologically targeted mitochondrial fission/fusion protect the brain against acute myocardial ischemia-reperfusion injury in prediabetic rats: The crosstalk between mitochondrial apoptosis and inflammation.

An imbalance of brain mitochondrial dynamics, increases in brain inflammation and apoptosis, and increasing cognitive dysfunction, have been reported as being associated with prediabetes and myocardial ischemia-reperfusion (IR) injury. Since inhibiting mitochondrial fission with Mdivi-1 or promoting fusion with M1 had cardioprotective effects in myocardial IR injury and obesity, the neuroprotective roles of Mdivi-1 and M1 when administered at different time points of myocardial IR injury in obese prediabetes have never been determined. Ninety-six male Wistar rats were fed with either a normal (ND: n = 8) or a high-fat diet to induce prediabetes (HFD: n = 88) for 12 weeks.

Acetylcholine receptor agonists effectively attenuated multiple program cell death pathways and improved left ventricular function in trastuzumab-induced cardiotoxicity in rats.

Aims: Cardiotoxicity is a seriously debilitating complication of trastuzumab (TRZ) therapy in patients with cancer as a consequence of overexpression of the human epidermal growth factor receptor 2. Although most TRZ-induced cardiotoxicity (TIC) cases are reversible, some patients experience chronic cardiac dysfunction, and these irreversible concepts may be associated with cardiomyocyte death. Acetylcholine receptor (AChR) activation has been shown to exert cardioprotection in several heart diseases, but the effects of AChR agonists against TIC have not been investigated.

Treatment with apoptosis inhibitor restores cognitive impairment in rats with myocardial infarction.

We previously reported that apoptosis is responsible for cognitive impairment in rats with myocardial infarction (MI). Acute administration of an apoptosis inhibitor (Z-vad) effectively reduced brain inflammation in rats with cardiac ischemia/reperfusion injury. However, the beneficial effects of Z-vad on cognitive function, brain inflammation, mitochondrial function, cell death pathways, and neurogenesis in MI rats have not been investigated.

Recent Advances in Mitochondrial Fission/Fusion-Targeted Therapy in Doxorubicin-Induced Cardiotoxicity.

Doxorubicin (DOX) has been recognized as one of the most effective chemotherapies and extensively used in the clinical settings of human cancer. However, DOX-mediated cardiotoxicity is known to compromise the clinical effectiveness of chemotherapy, resulting in cardiomyopathy and heart failure. Recently, accumulation of dysfunctional mitochondria via alteration of the mitochondrial fission/fusion dynamic processes has been identified as a potential mechanism underlying DOX cardiotoxicity.

Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury: Cumulative evidence for future cardioprotective strategies.

Cardiomyocyte death is one of the major mechanisms contributing to the development of myocardial infarction (MI) and myocardial ischemia/reperfusion (MI/R) injury. Due to the limited regenerative ability of cardiomyocytes, understanding the mechanisms of cardiomyocyte death is necessary. Pyroptosis, one of the regulated programmed cell death pathways, has recently been shown to play important roles in MI and MI/R injury.

Chitosan-coated oleaginous microalgae-fungal pellets for improved bioremediation of non-sterile secondary effluent and application in carbon dioxide sequestration in bubble column photobioreactors.

Oleaginous microalga Scenedesmus sp. SPP was rapidly immobilized in oleaginous fungal pellets by their opposite-surface-charges. Microalgae-fungal (MF) pellets were more effective in bioremediation of non-sterile secondary effluent than mono-culture.

GSDMD-mediated pyroptosis dominantly promotes left ventricular remodeling and dysfunction in post-myocardial infarction: a comparison across modes of programmed cell death and mitochondrial involvement.

Background: Myocardial infarction (MI) has recently accounted for more than one-third of global mortality. Multiple molecular pathological pathways, such as oxidative stress, inflammation, and mitochondrial dysfunction, have been recognized as possible mechanisms in the development of MI. Furthermore, different phases of ischemic injury following the progression of MI were also associated with multiple types of programmed cell death (PCDs), including apoptosis, necroptosis, ferroptosis, and pyroptosis.