Search Results (1,879)

Mitochondrial transplantation has been proposed as a strategy to restore cellular bioenergetics after oxidative injury, but the mechanisms governing ATP recovery remain unclear. Using placental mitochondria, we examined ATP restoration following H₂O₂-induced oxidative stress. Unmodified mitochondria modestly increased ATP under baseline conditions but failed to restore ATP after injury. In contrast, lipid-coated mitochondria (MitoCoat) and lipid-encapsulated mitochondria-associated mRNAs (MitoCoat–mRNA) significantly increased ATP levels in injured cells. Transcriptomic analyses revealed that ATP recovery occurred without the normalization of canonical glycolytic or oxidative phosphorylation (OXPHOS) gene programs. Instead, unmodified mitochondria induced broad transcriptional responses associated with immune activation and cellular stress, whereas MitoCoat elicited a more restricted transcriptional profile. Notably, mitochondria-associated mRNAs alone restored ATP without detectable changes in host transcriptional programs. The removal of mitochondrial surface-associated ribosomes or the inhibition of cytosolic but not mitochondrial translation attenuated ATP recovery. The restoration of key metabolic enzymes through cytosolic translation, including PFKP, pyruvate dehydrogenase, and ATP synthase subunit ATP5A suggests that mitochondria-associated mRNAs promote recovery by re-establishing coupling between glycolysis and mitochondrial OXPHOS. Together, these findings identify encapsulated mitochondria-associated mRNAs as a potential strategy to restore cellular bioenergetics under oxidative stress. Full article

Neurodegenerative diseases (NDDs) in children represent a heterogeneous group of rare but collectively significant disorders characterized by progressive neurological decline, developmental regression, and substantial morbidity and mortality. Unlike adult-onset neurodegeneration, pediatric conditions are predominantly genetic and frequently arise from defects in fundamental cellular pathways, including lysosomal degradation, mitochondrial oxidative phosphorylation, peroxisomal lipid metabolism, and myelin maintenance. This comprehensive review synthesizes current knowledge regarding the epidemiology, molecular classification, pathophysiology, and emerging therapeutic strategies of major pediatric neurodegenerative disorders. Epidemiological data indicate a “rare-but-many” landscape, where individually uncommon diseases collectively impose a measurable population burden. Mechanistically, disease progression reflects converging processes such as toxic substrate accumulation, impaired autophagy–lysosome flux, mitochondrial bioenergetic failure, oxidative stress, neuroinflammation, and glial dysfunction. Representative groups discussed include lysosomal storage disorders, leukodystrophies, mitochondrial encephalopathies, peroxisomal disorders, and other monogenic neurodegenerative syndromes. Advances in next-generation sequencing, metabolic profiling, and neuroimaging have substantially improved diagnostic accuracy and enabled earlier detection, including through newborn screening programs. Therapeutic paradigms are shifting from primarily supportive care toward mechanism-based interventions, including enzyme replacement therapy, hematopoietic stem cell transplantation, substrate reduction strategies, and gene therapy approaches. Early molecular diagnosis is increasingly recognized as critical for optimizing outcomes, particularly in disorders amenable to presymptomatic intervention. Continued integration of genomic medicine, standardized epidemiologic surveillance, and translational research will be essential to refine disease classification, improve prognostication, and expand access to targeted therapies. Collectively, pediatric neurodegenerative diseases exemplify the intersection of developmental neurobiology and inherited metabolic dysfunction, underscoring the need for multidisciplinary, precision-based clinical strategies. Full article

Pneumoconiosis, characterized by progressive pulmonary fibrosis, remains a predominant occupational disease in China, with coal workers’ pneumoconiosis (CWP) and silicosis being the primary subtypes. Despite extensive research, its underlying pathogenic mechanisms are not yet fully understood. Mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs) are crucial subcellular microdomains that govern Ca²⁺ transport, sustain cellular bioenergetics, and maintain systemic homeostasis. Emerging evidence has linked the structural and functional dysregulation of MAMs to the pathogenesis of various fibrotic disorders. Apoptosis, a highly regulated cell death process, is a key driver in pneumoconiosis progression, in which Ca²⁺ imbalance serves as a critical signaling cascade. Mitofusin 2 (MFN2), a core regulator of MAMs’ structural integrity, mediates mitochondrial fusion and directly bridges the ER with the outer mitochondrial membrane, thereby stabilizing ER–mitochondrial coupling. However, whether MFN2 mitigates fibrosis by preserving MAMs’ integrity and subsequently suppressing Ca²⁺-dependent apoptosis remains elusive. In this study, we established SD rat and A549 cell models of CWP. Our results demonstrated that MFN2 expression was downregulated after coal dust exposure, accompanied by MAMs impairment, Ca²⁺ imbalance, and increased apoptosis, which ultimately drove the pathological progression of pulmonary fibrosis. Notably, MFN2 overexpression restored MAMs’ structure and Ca²⁺ homeostasis, alleviated abnormal apoptosis, and subsequently inhibited fibrosis. This study highlights the importance of the MFN2–MAMs–Ca²⁺–apoptosis axis and identifies MFN2 as a potential therapeutic target for pneumoconiosis. Full article

Mitochondrial dysfunction is a relevant hallmark of Alzheimer’s disease (AD), contributing to the impaired metabolic homeostasis involved in neuronal loss and cognitive decline. In this study, we target the metabolic dysfunction occurring in AD through a novel pharmacological approach involving the modulation of glutamate dehydrogenase (GDH), which converts glutamate to α-ketoglutarate and supports the tricarboxylic acid (TCA) cycle. In our experimental models (i.e., differentiated SH-SY5Y cells and primary rat cortical neurons exposed to glyceraldehyde and amyloid-beta peptide 1-42, respectively), the allosteric GDH activator 2-Aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) increased mitochondrial ATP production, improved cellular bioenergetics, and reduced oxidative stress, ultimately promoting neuronal survival. Ionic dysfunctions in AD are linked to disrupted calcium homeostasis and organelle storing properties. In this context, GDH activation potentiated mitochondrial and endoplasmic reticulum calcium buffering capacity by enhancing store-operated calcium entry. Oxidative stress, largely driven by mitochondrial ROS overproduction, represents another major contributor to AD pathology. In our AD models BCH-mediated GDH activation reduced ROS formation and restored mitochondrial membrane potential (ΔΨ_m). Importantly, these metabolic and ionic improvements were associated with decreased accumulation of amyloid-β (Aβ_1-42) and phosphorylated tau (pTau), two key AD biomarkers. Overall, modulation of the GDH/TCA pathway represents a promising approach for restoring metabolic dysfunctions and counteracting oxidative stress and ionic dysregulation and therefore AD neurodegeneration. Full article

Muscle vulnerability occurs at both extremes of the human lifespan, although its biological significance differs substantially between developmental growth and late-life decline. During childhood and adolescence, insufficient muscle accretion reflects disruption of physiological anabolic trajectories driven by inadequate energy availability, inflammatory burden, endocrine imbalance, or disease-associated catabolism. In older adults, muscle deterioration is characterized by anabolic resistance, neuromuscular remodeling, chronic low-grade inflammation, and hormonal decline, culminating in sarcopenia and loss of functional independence. The absence of harmonized diagnostic frameworks across age groups limits direct translational extrapolation. A lifespan-informed perspective distinguishing growth-supportive from function-preserving nutritional approaches is, therefore, required. This narrative review examines how major classes of nutritional bioactive interact with molecular pathways regulating skeletal muscle homeostasis in fragile populations across the lifespan. The analysis encompasses energy adequacy, protein quantity and quality, amino acid-dependent anabolic signaling, vitamin D status, lipid-derived mediators, redox-modulating phytochemicals, and micronutrients supporting mitochondrial bioenergetics. In pediatric contexts, nutritional interventions primarily aim to restore anabolic permissiveness within a structurally intact growth environment. In aging individuals, strategies focus on mitigating anabolic resistance through optimized protein intake, correction of micronutrient insufficiencies, and integration with resistance exercise to preserve functional capacity. This narrative review emphasizes the need to distinguish mechanistic rationale from clinically validated interventions, as improvements in molecular pathways do not consistently translate into meaningful functional outcomes. Full article

The C-terminal binding protein 1 (CTBP1) is a transcriptional corepressor with a major role in nervous system growth and development. There are only 20 published cases with CTBP1 mutations, displaying a phenotype of Hypotonia, Ataxia, Developmental Delay and Tooth enamel defect Syndrome (HADDTS). Histochemical evidence of decreased mitochondrial respiratory chain activity has been previously reported, but comprehensive data on the metabolic phenotype assessed by various cellular respiration parameters are still missing. We present a 10-year-old female with typical HADDTS features, harboring the most reported de novo heterozygous CTBP1 mutation c.991C>T. To elucidate her metabolic phenotype, we quantified mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) utilizing an analyzer for assessing mitochondrial function (Seahorse XFp). Real-time metabolic assays revealed profound mitochondrial dysfunction with significantly attenuated maximal respiration and spare respiratory capacity compared to neurotypical controls. Following mitochondria-targeted nutritional support for one-year measurable bioenergetic improvements and reduced number of respiratory infections were registered. However, neurological recovery and new skill acquisition were not observed. We present a novel case of CTBP1-related neurodevelopmental disorder and demonstrate, for the first time, the application of non-invasive, real-time mitochondrial functional assessment in this setting, providing additional evidence for mitochondrial dysfunction in HADDTS. Full article

Mitochondrial dysfunction is a hallmark of aging and age-related physical decline in people living with HIV (PLWH) who experience accelerated aging. This pilot study investigated the relationships between platelet mitochondrial function, physical performance, and body composition in older, sedentary PLWH compared with older, sedentary HIV-negative controls. Platelets have the potential to act as minimally invasive and easily accessible biomarkers for systemic mitochondrial bioenergetics and may serve as a practical biomarker in aging-related research. We analyzed correlations between mitochondrial parameters, protein levels, and measures of physical performance and body composition in a cohort of predominantly African American men (n = 7 PLWH, n = 7 controls). Body composition was assessed using dual-energy X-ray absorptiometry (DXA), and exercise capacity through VO₂ peak and strength tests. Platelet mitochondrial bioenergetic parameters were measured by oxygen consumption rates (OCR) and extracellular acidification rates (ECAR). Key mitochondrial proteins SIRT3, COXII, DRP1, and OPA1 were evaluated by Western blotting. The PLWH and HIV-negative control groups were similar in age and cardiorespiratory fitness. In PLWH, basal OCR and ATP-linked respiration showed strong positive correlations with VO₂ peak (r = 0.874, p < 0.05 and r = 0.862, p < 0.05, respectively) and negative correlations with BMI (r = −0.856, p < 0.05 and r = −0.849, p < 0.05, respectively). SIRT3 emerged as a potential key player, demonstrating strong positive correlations with basal OCR (r = 0.804, p < 0.05), ATP-linked respiration (r = 0.787, p < 0.05), and VO₂ peak (r = 0.970, p < 0.001), and negative correlations with BMI (r = −0.830, p < 0.05) and fat mass (r = −0.827, p < 0.05) in PLWH. Analyses focused on within-group associations in PLWH because bioenergetic measures were obtained using different Seahorse platforms in PLWH and controls, precluding valid direct quantitative comparisons between groups. Our findings provide evidence for significant associations between platelet mitochondrial bioenergetics, specific mitochondrial proteins (particularly SIRT3), and key physical attributes in older, sedentary PLWH. These preliminary findings suggest that platelets may serve as minimally invasive biomarkers of systemic mitochondrial health, contribute to our understanding of mitochondrial function in HIV-associated accelerated aging, and inform future interventions to enhance mitochondrial function and improve health outcomes in this vulnerable population. However, results should be interpreted cautiously given the small sample size and exploratory design and should be considered hypothesis-generating rather than definitive. Larger, demographically more diverse studies that include HIV-negative controls are needed to validate these associations and determine their clinical relevance. Full article

Porcine organotypic retinal explant cultures are widely used to study retinal neurodegeneration under controlled conditions, but the biological processes that occur in the retinal explant over time due to preparation-induced injury and culture are not well understood. Here, we generated a time-resolved transcriptomic reference for porcine neural retinal explants, which were maintained ex vivo for 10 days. Global expression profiles are strongly separated by culture time, with Day 0 clearly distinct from cultured samples and Day 7 and Day 10 showing the highest similarity, indicating a transition toward a later stabilized state. Across the time course, 3187 genes were differentially expressed relative to Day 0, with the largest shifts occurring at an early stage of culture (Day 1–Day 3). Pathway-level analyses revealed coordinated remodeling involving inflammatory signaling and metabolic/bioenergetic changes, including reduced mitochondrial and oxidative phosphorylation-related programs at later time points. Here, we provide a time-resolved transcriptomics reference dataset for cultured porcine retinal explants. These data can build a foundation to interpret data generated in this model, differentiate changes inherent to the explant culture from treatment-specific effects and select appropriate experimental windows for mechanistic studies of retinal degeneration. Full article

This work introduces an approach to evolutionary analysis in which information encoded in amino-acid sequences is converted into a specific type of image, termed a genetic image. Genetic images derived from the amino-acid sequences of cytochrome b and cytochrome c oxidase subunit I are shown to be suitable for identifying evolutionary similarities between organisms. Furthermore, artificial neural networks are demonstrated to recognize these genetic images, enabling identification of species evolution. The results indicate the similarity of the genetic images of organisms belonging to species that emerged earlier during Earth’s evolutionary history to the genetic images of organisms belonging to species that emerged later. This finding indicates that genetic images are inherited and undergo gradual modification during evolutionary processes. The phenomenon of inheritance and modification of genetic images suggests that evolution tends to change the already existing functionalities of organisms, which allows for the ordering of organisms belonging to different species from ancient forms, through species that appeared successively during evolution, to those belonging to species that have developed more recently, up to Homo sapiens. Moreover, unlike analyses based on phylogenetic trees, the method presented in this article does not require computing hypothetical taxonomic units to study evolution. Combined with analyses of the inheritance of genetic images, it can support the interpretations of phylogenetic trees and evolutionary research. Full article

Saline–alkali stress severely limits crop production worldwide. Soybean [Glycine max (L.) Merr.] is particularly sensitive during seed germination, a stage critical for stand establishment. This complex stress environment encompasses two distinct yet equally critical dimensions: neutral salt stress and alkaline salt stress, each eliciting specialized physiological and metabolic responses. Here, a comparative assessment of four genotypes (tolerant: CN16, CN17; sensitive: Williams 82, K18) under 100 mmol/L Na⁺ revealed that alkaline salt stress exerts a significantly more potent inhibitory effect than neutral salt stress. Tolerant cultivars maintained 75–80% germination under alkaline conditions, whereas sensitive ones dropped below 15%, a divergence primarily driven by superior oxidative mitigation capacity. Integrated multi-omics analysis of the tolerant variety CN16 identified stage-specific regulatory shifts: early alkaline salt stress (60 h) triggers extensive transcriptional reprogramming focused on physical barrier reinforcement, including cell walls and lipid remodeling. By 96 h, regulatory modes between the two stress types diverged: neutral salt elicited a transcriptional surge, while alkaline salt transitioned to a metabolically dominant regulation, shifting flux from growth-related isoflavonoids to defense-related anthocyanins. Crucially, this study uncovers the distinct bioenergetic trade-offs governing these responses: whereas adaptation to neutral salt relies on low-energy galactose metabolism, tolerance to alkaline salt demands energy-intensive processes, specifically the active vacuolar compartmentalization of organic acids and anthocyanins for intracellular buffering. This obligatory energy expenditure restricts biomass accumulation, explaining the severe growth penalties observed in complex saline-alkali environments. Finally, the identification of a core regulatory module driven by key genes, including GmPHOT2b, GmLOG, and GmSHMT08, enriches the metabolic regulatory network under saline-alkali stress, providing core targets and a theoretical framework for precisely balancing metabolic expenditure with biomass accumulation in breeding practice. Full article

Fanconi anemia (FA) is a rare inherited disorder classically defined by defective DNA interstrand crosslink repair, leading to bone marrow failure and cancer predisposition. Increasing evidence indicates that FA pathophysiology extends beyond genomic instability to include mitochondrial dysfunction, oxidative stress, and impaired antioxidant responses. Across multiple cellular models and patient-derived samples, FA cells display altered mitochondrial bioenergetics, increased reactive oxygen species (ROS) production, and defective activation of redox-adaptive pathways, contributing to cumulative damage to DNA, lipids, and proteins. These alterations are particularly relevant in hematopoietic stem and progenitor cells, where metabolic stress and redox imbalance amplify stem cell exhaustion. Current data support a bidirectional interplay in which mitochondrial dysfunction and oxidative stress act mainly as secondary but amplifying factors of the primary DNA repair defect, establishing pathogenic feedback loops. Preclinical studies suggest that modulation of redox balance and mitochondrial function may improve cellular homeostasis, and early clinical investigations of antioxidant strategies indicate acceptable safety and measurable effects on oxidative biomarkers. However, clinical evidence remains limited and heterogeneous, with uncertain impact on long-term disease progression. Moreover, most mechanistic insights derive from in vitro or patient-derived models, while animal models and longitudinal clinical studies remain insufficient. Overall, a more integrated and translational framework is needed to clarify causality, validate biomarkers, and define the therapeutic potential of targeting metabolic and redox pathways in FA. Full article

Colorectal cancer (CRC) is a multifactorial disease influenced by genetic and environmental factors. The endothelial nitric oxide synthase (eNOS) gene, involved in nitric oxide (NO) production, is associated with carcinogenesis. This study aimed to evaluate the association between eNOS −786T>C and G894T polymorphisms and CRC susceptibility in an Algerian population. Genotype and allele frequencies were analyzed, and associations were assessed using odds ratios (ORs) and 95% confidence intervals (CIs). For −786T>C polymorphism, the CC genotype was significantly more frequent in patients than in controls (37.33% vs. 21.67%) and was associated with increased risk of CRC (OR = 2.15, 95% CI: 1.21–3.88, p = 0.004), whereas the TT genotype showed a protective effect (OR = 0.41, 95% CI: 0.20–0.81, p = 0.005). Regarding the G894T polymorphism, the TT genotype was significantly associated with increased susceptibility to CRC (44.67% vs. 8.33%; OR = 8.88, 95% CI: 4.19–15.40, p < 0.001), while the GG genotype was protective (OR = 0.18, 95% CI: 0.10–0.32, p < 0.001). Allelic analysis confirmed that the C and T alleles were risk factors. Furthermore, eNOS polymorphisms were significantly associated with tumor location. In conclusion, the eNOS −786T>C and G894T polymorphisms are significantly associated with CRC susceptibility in the Algerian population and could serve as potential genetic biomarkers. Full article

(1) Background: Mild traumatic brain injury (mTBI), the most prevalent form of traumatic brain injury, often results from repetitive impacts to the head and is associated with long-term neurological impairment. The pathophysiology of mTBI is multifactorial and involves alterations in mitochondrial bioenergetics, a key determinant of neuronal function and survival. Although mitochondrial dysfunction is recognized as a hallmark of mTBI, its long-term effects on bioenergetics and the roles of regulatory cytosolic and mitochondrial proteins remain poorly understood. We hypothesized that repeated mTBI (rmTBI) induces sustained deficits in mitochondrial bioenergetics that are associated with long-term changes in key bioenergetic and other regulatory proteins. (2) Methods: Using the repeated CHIMERA injury model in adult male rats, randomly assigned to sham or rmTBI groups, we assessed mitochondrial respiration in isolated mitochondria and whole cerebral cortex homogenates using a Clark O₂ electrode and an Oroboros O₂k respirometer at time points ranging from 1 day to 2 months post-injury. Western blotting was performed for expression of regulatory proteins HKI, DRP1, MFN2, VDAC1, and ANT2. (3) Results: At 2 months post-rmTBI, respiration was faster and uncoupled, while ATP synthesis was significantly slowed compared with sham rats. This was accompanied by decreased expression of mitochondrial MFN2 and ANT2, by increased mitochondrial expression of DRP1, and by decreased translocation of HKI to mitochondria. There was no significant difference in VDAC1 expression. Earlier time points showed no significant differences in bioenergetics or protein expression, but neuro-inflammatory markers (GFAP and Iba1) were significantly elevated at these earlier time points of post-injury. (4) Conclusions: These findings indicate that rmTBI leads to a delayed long-term impairment of mitochondrial bioenergetics associated with alterations in proteins critical for bioenergetic regulation and mitochondrial control. This suggests a pathophysiologic mechanism for the persistent cognitive and behavioral deficits observed following rmTBI. Full article

Background and Objectives: Tamoxifen, a cornerstone selective estrogen receptor modulator in breast cancer therapy, is increasingly recognized to be associated with retinal toxicity characterized by mitochondrial dysfunction, oxidative stress, lipid peroxidation, and oxidative DNA injury. By targeting mitochondrial bioenergetic dysfunction and redox disequilibrium, adenosine triphosphate (ATP) emerges as a biologically plausible candidate for retinal cytoprotection. This study aimed to evaluate the protective effect of ATP against tamoxifen-induced retinal toxicity in a rat model. Materials and Methods: Twenty-four male albino Wistar rats were randomly assigned to four groups: healthy control (HG), ATP-alone (ATPG, 4 mg/kg, intraperitoneally), tamoxifen-alone (TAMG, 5 mg/kg, orally), and tamoxifen plus ATP-treated (ATAG; ATP, 4 mg/kg, intraperitoneally; tamoxifen, 5 mg/kg, orally). Treatments were administered once daily for 30 days. Oxidative stress markers (malondialdehyde, total glutathione), antioxidant enzyme activities (superoxide dismutase, catalase), and oxidative DNA damage (8-hydroxy-2′-deoxyguanosine) were assessed in ocular tissues. Retinal histopathological evaluation included hematoxylin–eosin staining with semiquantitative assessment of edema, vascular congestion, polymorphonuclear leukocyte infiltration, and cytoplasmic vacuolization, together with quantitative measurements of retinal layer thicknesses and ganglion cell layer (GCL) cell counts. Results: Tamoxifen administration induced marked oxidative stress, antioxidant depletion, and increased oxidative DNA damage in ocular tissues, accompanied by significant thickening of retinal layers, reduced GCL cell counts, and pronounced disruption of retinal architecture. By comparison, ATP co-administration significantly suppressed lipid peroxidation and restored antioxidant defenses, thereby reducing oxidative DNA damage and preserving retinal structural integrity, as reflected by partial normalization of retinal layer thicknesses, preservation of GCL cell counts, and the presence of only mild residual edema. Conclusions: These findings indicate that ATP attenuates tamoxifen-induced retinal toxicity by supporting mitochondrial energy balance and redox homeostasis. Accordingly, ATP administration may represent a promising protective approach for reducing retinal injury associated with long-term tamoxifen therapy. Full article

Phospholipid transfer protein (PLTP) is a lipid transfer protein classically studied in the context of plasma lipoprotein metabolism, high-density lipoprotein (HDL) remodeling, and cardiovascular disease risk. PLTP facilitates phospholipid transfer between lipoproteins and regulates HDL particle size and composition through interactions with apolipoprotein A-I and apolipoprotein A-II. While its systemic roles in cholesterol handling, reverse cholesterol transport, and inflammatory signaling are well established, the cell-autonomous functions of PLTP within cardiomyocytes remain poorly defined, particularly in human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). Extensive experimental and clinical studies demonstrate that PLTP enhances ABCA1-dependent cholesterol efflux primarily by stabilizing ABCA1 at the plasma membrane and by promoting the generation of lipid-poor apolipoprotein A-I and pre-β HDL particles, which serve as efficient cholesterol acceptors; the magnitude of these effects depends on cellular context, PLTP expression levels, and the availability of lipid acceptors. PLTP expression is metabolically regulated and widely distributed across tissues, including macrophages and other non-hepatic cells, supporting roles beyond circulating lipoprotein remodeling. Altered PLTP activity has been linked to atherosclerosis, cardiovascular disease, and inflammatory pathways, underscoring its relevance to cardiac pathophysiology. Emerging evidence further suggests that intracellular cholesterol distribution, rather than total cholesterol content alone, critically influences mitochondrial membrane composition, bioenergetics, and stress signaling in cardiomyocytes. These observations raise the possibility that PLTP-regulated lipid flux may indirectly shape mitochondrial function by modulating cellular cholesterol homeostasis. This review synthesizes current knowledge of PLTP biology, cholesterol metabolism, and lipoprotein remodeling, and integrates these concepts with emerging frameworks in cardiomyocyte lipid metabolism and mitochondrial physiology. We highlight human iPSC-derived cardiomyocytes as a strategic and translationally relevant platform to investigate PLTP’s non-canonical, cell-intrinsic roles, identify critical knowledge gaps, and propose future directions for elucidating how PLTP may influence mitochondrial function in human cardiac cells. Full article