Biology subjects

Jia, Z.

Publications and source records attributed to Jia, Z..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

Essential Role of MHC II in the Antitubercular Efficacy of Pyrazinamide

Antibacterial drug mechanisms have traditionally been examined through a drug-pathogen lens, often overlooking the hosts role in shaping drug activity. However, growing evidence suggests that the host environment is crucial for antibacterial efficacy. Pyrazinamide (PZA), a key component of modern tuberculosis therapy, exemplifies this complexity--exhibiting potent in vivo activity despite its inability to reduce Mycobacterium tuberculosis viability in standard in vitro culture. Here, using macrophage and murine infection models, we identify a critical role for host cell-mediated immunity in PZAs antitubercular action. Through the use of MHC II knockout mice, we demonstrate that CD4 T cell help is essential for PZA efficacy. Notably, while IFN-{gamma} is required for PZA-mediated clearance of M. tuberculosis at extrapulmonary sites, bacterial reduction in the lungs occurs independently of IFN-{gamma} signaling. Additionally, we show that PZA leverages cell-mediated immunity in part through activation of the oxidative burst. Our findings underscore the need to incorporate host factors into antibacterial drug evaluation and highlight potential avenues for host-directed therapies and adjunctive antibiotics in first- and second-line tuberculosis treatment.

microbiology↗

bioRxiv2025

Tau deletion results in sex-dependent modulation of synaptic weakening in rat hippocampus

Tangles, a defining characteristic of Alzheimers disease (AD), are composed principally of hyperphosphorylated and misfolded tau species. However, dysregulation of tau precedes tangle formation by many years and is associated with cognitive decline, the best functional correlate of which is synaptic weakening and eventual synaptic loss. Although tau is present at synapses, its normal synaptic function is poorly understood - information vital to the rational development of tau-modifying therapies. Since rats have a greater cognitive repertoire than mice and display more robust signs of tau pathology in AD models, we developed a tau knockout (Mapt-/-) rat to investigate the impact of tau elimination on synaptic function. We observed that long-term depression (LTD), a form of synaptic weakening, is enhanced in the hippocampus of male, but not female, rats. This enhanced LTD was dependent on the synaptic activation of group I metabotropic glutamate receptors and involved altered synaptic actin polymerization. These studies therefore provide mechanistic insights into how tau modulates synaptic function via regulation of the actin cytoskeleton. Our findings are relevant to the understanding of the physiological roles of synaptic tau, the functional consequences of tau-lowering therapies, and the influence of sex in AD susceptibility.

neuroscience↗

bioRxiv2025

Single-cell transcriptome sequencing for opening the blood-brain barrier through specific mode electroacupuncture stimulation

BackgroundThe blood-brain barrier (BBB) interferes with the treatment of central nervous system disorders owing to the complexity of its structure and restrictive function. Thus, it is challenging to develop central nervous system drug delivery strategies. Specific mode electroacupuncture (EA) stimulation can effectively open the BBB in rats. MethodsHere, we used single-cell RNA sequencing (scRNA-seq) to comprehensively map the cell population in the Sprague-Dawley rat cerebral cortex. ResultsWe identified 23 cell subsets and eight types of cells in the brain by cell annotation. scRNA-seq revealed transcriptional changes in the cerebral cortex under EA. ConclusionsOur findings offer valuable insights into the molecular and cellular modifications in the brain resulting from EA intervention and serve as a resource for drug delivery across healthy and diseased states. Innovative approaches to enhance BBB opening will lead to more effective therapeutic plans and enhanced drug delivery.

neuroscience↗

bioRxiv2025

Evolution of hunt, kill, devour in a Vibrio ecospecies

Understanding the molecular and evolutionary basis of adaptation is a central challenge in biology. We have recently identified bacterial "ecospecies": strains that share a well-mixed gene pool with the rest of the species in most of the genome, but carry nearly fixed differences in [~]100 coadapted genes. We hypothesized this structure reflects ecological selection, but ecospecies have so far been characterized only genomically. Here, using "Molassodon" of the marine bacterium Vibrio parahaemolyticus, we provide first experimental evidence linking a multilocus ecospecies genotype to a laboratory phenotype. We find that Molassodon swimming in viscous environments is enhanced by differentiated lateral flagella that no longer drive surface swarming. Using Tn-seq, RNA-seq, and molecular genetics, we link differentiated Type VI secretion and nutrient uptake genes to the swimming phenotype, potentially invoking a natural adaptation related to "hunting". We also identify a convergent genotype also linking lateral flagella and nutrient uptake, suggesting ecological differentiation in V. parahaemolyticus occurs along recurring phenotypic axes and involves borrowing traits from a broader Vibrio gene pool. Together, our results provide first experimental evidence that ecospecies are functionally coherent units and illustrate how they can provide a window into the complex adaptations that shape bacterial ecology.

microbiology↗

bioRxiv2025

Ketone body driven lipid remodeling supports thermogenic adaptation to fasting

Metabolic adaptation to fasting may have conferred survival advantage to early humans and predicts weight gain caused by overnutrition in modern societies. Fasting suppresses brown adipose tissue (BAT) thermogenesis; however, it is unclear how BAT rewires cellular metabolism to balance between energy conservation and heat generation. Here, we report that BAT in mice under fasting and cold challenge consumed ketone bodies, specifically acetoacetate (AcAc). Ablating liver ketogenesis decreased, while enhancing hepatic AcAc output defended, body temperature in mice facing the dual challenge. Using stable isotope tracing in brown adipocytes in vitro combined with quantitative analysis of metabolic fluxes and lipidomics in BAT from genetic mouse models, we disentangled the two metabolic fates of AcAc - terminal oxidation in the mitochondria and lipid biosynthesis in the cytosol. Notably, AcAc-sourced carbon preferentially supported polyunsaturated fatty acid synthesis in BAT, linking to the positive impact of intermittent fasting on lipid profiles in both mice and humans. Therefore, ketone body utilization by thermogenic adipocytes contributes to metabolic resilience of mammals and can be targeted to optimize benefits of dietary regimens.

physiology↗

bioRxiv2025

Central nervous system atlas of larval zebrafish constructed using the morphology of single excitatory and inhibitory neurons

Single-neuron morphology mapping is fundamental for deciphering brain architecture and function, yet in vertebrates it remains limited in spatial coverage and cell-type information. Here we present a nervous system-wide single-neuron morphology atlas of larval zebrafish with annotated excitatory/inhibitory identity and dendrite-axon polarity. The atlas comprises >20,000 reconstructed neurons from >13,400 animals, spanning the central and peripheral nervous system and representing [~]24.5% of the total excitatory and inhibitory neurons in the brain, all integrated into a common physical space with neuroanatomical parcellations. We define >500 excitatory and inhibitory neuronal morphotypes and construct putative inter-cell-type and interregional connectomes. Projection and morphotype analyses reveal distinct laterality and directionality biases and modular innervation patterns in excitatory and inhibitory neurons, while network analyses uncover fundamental connectivity motifs, hubs, and sensorimotor pathways. Accessible through custom-built interactive platform ZExplorer, this atlas provides a foundational resource for multimodal data integration, circuit analysis, computational modeling, and hypothesis-driven research.

neuroscience↗

bioRxiv2025

N1 cassette-lacking NMDA receptors mediate the antidepressant activity of ketamine

Ketamine has emerged as a rapid-acting and robust antidepressant1,2. However, the mechanism of its antidepressant action remains enigmatic. The core issue that has yet to be resolved is whether NMDA receptors (NMDARs), which are subject to open channel blockade by ketamine3,4, mediate the antidepressant effect. NMDARs naturally undergo alternative splicing of the obligatory GluN1 subunit5, producing receptor diversity in the brain that has not been considered in the actions of ketamine. Here we discover that alternative splicing of Grin1 exon 5, which leads to exclusion (GluN1a) or inclusion (GluN1b) of the N1 cassette, located in the N-terminal domain of GluN1 distant from the pore, unexpectedly dictates the level and dynamics of NMDAR blockade by ketamine and gates its antidepressant activity. We find that ketamine prevents NMDAR-dependent long-term potentiation (LTP) in the CA1 region of the hippocampus in mice engineered to exclude Grin1 exon 5 (GluN1a mice), but ketamine has no effect on LTP in mice engineered to include this exon (GluN1b mice). Ketamine inhibits synaptic NMDARs in CA1 pyramidal neurons in both GluN1a and GluN1b mice, with the level of steady-state blockade marginally greater in GluN1a- than in GluN1b-containing NMDARs. However, the rate of relief of ketamine blockade upon membrane depolarization is markedly slower in GluN1a than in GluN1b neurons such that GluN1a-containing receptors remain blocked during bursting activity, whereas those containing GluN1b escape the ketamine blockade. Furthermore, ketamine treatment, either via systemic administration or local infusion into the hippocampus, induces an antidepressant effect in GluN1a mice but has no effect in GluN1b mice. Collectively, we identify GluN1a-containing NMDARs, which are persistently blocked by ketamine during neuronal firing activity, to be selectively responsible for the antidepressant effect.

neuroscience↗

bioRxiv2025

A zebrafish immunodeficiency model induced by the combination of Tacrolimus and Everolimus for rapid assessment of immune-enhancing agents

A methodology for the assessment of the immune-enhancing effects of various substances within a period of 5 days was reported. Experimentally, it was determined that the continuous treatment of Tacrollimus (0.5 ng/mL) and Everolimus (5 g/mL) on zebrafish from 48 hpf to 120 hpf was sufficient to establish an immunodeficient model. The results showed that the model exhibited a significant reduction in the number of immune cells (thymocytes, myeloid cells, and macrophages) and a greater than 50% decrease in the expression of immune-related genes (itk, hexb, cpa5, isg15, rsad2). Astragalus powder can effectively increase the content of thymic T cells and macrophages, but its effect on myeloid cells is limited. Ganoderma lucidum spore powder had the most obvious influence on macrophages, with limited impact on thymus cells and myeloid cells. Royal jelly showed a significant effect on thymus T cells and macrophages, but its effect on myeloid cells was limited. Bailing capsule can significantly increase the content of myeloid cells and thymus T cells, while its effect on macrophages was limited. The study showed immune indexes varied in recovery with different immunomodulators versus the model group, suggesting they may act via distinct mechanisms. Summary StatementA robust immune system is vital to overall health and quality of life. Recent years have witnessed surging development of immune-boosting pharmaceuticals, nutraceuticals, and functional foods. However, an easy-to-use, rapid and intuitive immunity assessment framework is still missing. Here, a methodology for the assessment of the immune-enhancing effects of various substances within a period of 5 days was reported.

immunology↗

bioRxiv2025

Multiple evolutionary events in host plant adaptation in Lepidoptera

The evolution of insect host adaptation is a key component of insect-plant coevolution, a complex process often shaped by multiple evolutionary events. In this study, we identified two UDP-glycosyltransferase (UGT) genes, SfruUGT33T10 and SfruUGT33F32, in the fall armyworm Spodoptera frugiperda, which play critical roles in the tolerance of benzoxazinoids (BXs), secondary metabolites in maize. These two detoxification enzymes exhibited distinct glycosylation patterns for BXs and varying detoxification efficiencies, reflecting independent evolutionary trajectories. Phylogenetic analyses revealed that SfruUGT33T10 originated independently within Noctuidae, while SfruUGT33F32 resulted from tandem duplication within the UGT33F gene family and may have undergone neofunctionalization within the Spodoptera genus. Our findings provide evidence that the evolution of these two UGT paralogs contributed to the variation in the tolerance to maize BXs among different Lepidopteran species. This research underscores the significance of multiple independent evolutionary routes in host plant adaptation and offer new insights into the complex evolutionary processes underlying insect-plant interactions.

evolutionary biology↗

bioRxiv2025

SMART: an approach for accurate formula assignment in spatially-resolved metabolomics

Spatially-resolved metabolomics plays a critical role in unraveling tissue-specific metabolic complexities. Despite its significance, this profound technology generates thousands of features, yet accurate annotation significantly lags behind LC-MS-based approaches. To bridge this gap, we introduce SMART, an open-source platform designed for precise formula assignment in mass spectrometry imaging. SMART constructs a KnownSet database containing 2.8 million formulas linked by DBEdges derived from repositories such as HMDB, ChEMBL, PubChem, and BioEdges from KEGG biological reactant pairs. Using a multiple linear regression model, SMART extracts formula networks associated with the m/z of interest and scores potential candidates based on several criteria, including linked formulas, DBEdges/BioEdges, and ppm values. Benchmarking against reference datasets demonstrates that SMART achieves prediction accuracy rates of up to 92.4%. Applied to mass spectrometry imaging, SMART successfully annotated 986 formulas in developing mouse embryos. This robust platform enables systematic formula annotation within tissues, enhancing our understanding of metabolic heterogeneity.

bioinformatics↗

bioRxiv2025

Intrinsic Opening of BK Channels Derives from Inherent Leakage in Hydrophobic Gating

The big potassium (BK) channels remain open with a small limiting probability of Po [~] 10-7 at minimal Ca2+ and negative voltages < -100 mV. The molecular origin and functional significance of such "intrinsic opening" are not understood. Here we combine atomistic simulations and electrophysiological experiments to show that the intrinsic opening of BK channels is an inherent property of the vapor barrier, generated by hydrophobic dewetting of the BK inner pore in the deactivated state. The vapor barrier only gives rise to a finite free energy barrier, of [~] 8 kcal/mol, and cannot completely shut down K+ flow even when the voltage sensor domains are fully deactivated. This results in the leaking currents that can be measured at negative voltages as the indication of intrinsic opening. The shallow limiting slope of Po at negative voltages results primarily from the electric field effects on the permeating ion through the vapor barrier. We further demonstrate that the vapor barrier can be perturbed by inner pore mutations and truncation of the cytosolic domains, leading to predicable changes in limiting slope measurements. Therefore, the intrinsic opening in BK channels, and possibly in other ion channels, opens up an opportunity to experimentally study hydrophobic gating. Our results further suggest that intrinsic opening in BK channels is the fundamental basis for the allosteric mechanism of activation by both voltage and Ca2+.

biophysics↗

bioRxiv2025

Atomistic Simulation of Voltage Activation of a Truncated BK Channel

Voltage-dependence gating of ion channels underlies numerous physiological and pathophysiological processes, and disruption of normal voltage gating is the cause of many channelopathies. Here, long timescale atomistic simulations were performed to directly probe voltage-induced gating transitions of the big potassium (BK) channels, where the voltage sensor domain (VSD) movement has been suggested to be distinct from that of canonical Kv channels but remains poorly understood. Using a Core-MT construct without the gating ring, multiple voltage activation transitions were observed at 750 mV, allowing detailed analysis of the activated state of BK VSD and key mechanistic features. Even though the S4 helix remains the principal voltage sensor in BK, its vertical displacement is only [~]3 [A] and accompanied by significant lateral movements. The nature of the predicted VSD movement is in strong agreement with recent Cryo-EM structural studies of mutant BK channels with constitutively activated VSD. Free energy analysis based on the predicted activation transition yielded a total gating charge of 0.44 e per VSD, consistent with the experimental range of 0.48 - 0.65 e. We further show that the ability of modest physical movements with a small total gating charge to drive effective voltage gating of BK can be attributed to large gradients in the local electric field as reshaped by the protein. Furthermore, the S4 movement is coupled to the pore opening through a non-canonical pathway that involves the tightly packed S4-S5-S6 interface. These distinct mechanistic features may be relevant to voltage gating of other ion channels where VSDs are not domain-swapped with respect to the pore-gate domain. Significance StatementThe big potassium (BK) channel is the only potassium channel that integrates intracellular calcium signaling with membrane depolarization. It is considered one of the most important channels in cardiovascular and neurological disorders. It has been known that voltage gating of BK channels has distinct features compared to the canonical voltage gating mechanism established through studies of voltage-gated potassium (Kv) channels. Yet, little is known about the molecular nature of voltage sensing and pore activation of BK channels at present. Our work reports the first successful direct simulation of voltage-dependent activation of the big potassium (BK) channel, revealing novel voltage sensing and sensor-pore coupling mechanisms that have largely eluded the community until now.

biophysics↗

bioRxiv2024

Polyphosphate as a Novel Regulator of Super-Enhancer Complexes: Disruption of Phase Separation and Gene Expression

Inorganic polyphosphate (polyP) is a highly conserved linear polymer of orthophosphate, present across nearly all living organisms. Its functional diversity, particularly through recently discovered post-translational modifications, has garnered increasing scientific interest. However, its role in gene regulation, especially in mammalian systems, remains unexplored. In this study, we present findings that demonstrate that polyP multi-targets the super-enhancer complex to regulate gene expression, marking a novel mechanism of transcriptional control. We show that polyP modifies key components of the complex, including the Mediator subunit MED1, the coactivator Bromodomain-containing protein 4 (BRD4), and the transcriptional regulator Yin Yang 1 (YY1). This polyP-mediated modification not only disrupts their ability to undergo phase separation but also downregulates the expression of MED1 and BRD4, as well as impairs the nuclear localization of YY1. Furthermore, polyP inhibits YY1 dimer formation and disrupts YY1-mediated DNA looping, leading to suppressed gene expression. These discoveries highlight polyP as a novel regulator of super-enhancer-driven gene transcription and provide new insights into the broader role of polyP in epigenetic regulation. This work uncovers a previously unknown layer of gene control, positioning polyP as a critical player in transcriptional regulation through its interaction with transcription factors and coactivators. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=147 SRC="FIGDIR/small/628164v1_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@10b53b2org.highwire.dtl.DTLVardef@a3dc10org.highwire.dtl.DTLVardef@1c4d72forg.highwire.dtl.DTLVardef@b7378_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIPolyP modifies key components of the super-enhancer complex BRD4, MED1 and YY1 by targeting their His-rich, Lys-rich or PASK sequences C_LIO_LIPolyP disrupts phase separation of BRD4, MED1 and YY1 C_LIO_LIPolyP impairs YY1s recruitment of BRD4 and MED1 and disrupts nuclear localization, dimerization, DNA looping and DNA binding to YY1 C_LIO_LIPolyP attenuates gene expression mediated by YY1 and BRD4 C_LI

molecular biology↗

bioRxiv2024

Development of a De Novo Protein Binder that Inhibits the Alpha Kinase eEF2K

Elongation factor 2 kinase (eEF2K) is calmodulin activated and phosphorylates eEF2, a GTPase, that regulates global translation. When eEF2K phosphorylates eEF2, protein translation is halted. This process may be critical to studying how diseases like cancer dysregulate protein synthesis. eEF2K is an alpha kinase and not targeted by conventional kinase inhibitors. Traditional methods of structure-based drug design are incredibly time consuming and expensive, which may involve screening large libraries of small molecules. We have generated de novo small binder proteins ([~]10kDa) - using RFDiffusion and ProteinMPNN. One promising de novo binder protein we produced, CAM1 binds to a hydrophobic patch on the calmodulin binding domain of eEF2K with nanomolar affinity as determined by isothermal titration calorimetry. This binder, in vitro, significantly reduces eEF2 peptide phosphorylation, comparable to the gold-standard small molecule eEF2K inhibitor, A-484954. The predicted structure of CAM1 is a helical bundle which has been confirmed by circular dichroism spectroscopy. Impressively, CAM1 has a melting temperature >800C, and is produced recombinantly in bacteria, greater than 5 mg / culture liter. We have also determined that CAM1 transfection significantly reduces mammalian HeLa cell proliferation comparable to A-484954 treatment and inhibits the phosphorylation of eEF2. Our de novo binder, the first to our knowledge to inhibit an alpha kinase, and the first non-competitive eEF2K inhibitor, establishes an alternative method of targeting atypical kinase activity.

biochemistry↗

bioRxiv2024

A trans-translation inhibitor is potentiated by zinc and kills Mycobacterium tuberculosis and non-tuberculous mycobacteria

Mycobacterium tuberculosis poses a serious challenge for human health, and new antibiotics with novel targets are needed. Here we demonstrate that an acylaminooxadiazole, MBX-4132, specifically inhibits the trans-translation ribosome rescue pathway to kill M. tuberculosis. Our data demonstrate that MBX-4132 is bactericidal against multiple pathogenic mycobacterial species and kills M. tuberculosis in macrophages. We also show that acylaminooxadiazole activity is antagonized by iron but is potentiated by zinc. Our transcriptomic data reveals dysregulation of multiple metal homeostasis pathways after exposure to MBX-4132. Furthermore, we see differential expression of genes related to zinc sensing and efflux when trans-translation is inhibited. Taken together, these data suggest that there is a link between disturbing intracellular metal levels and acylaminooxadiazole-mediated inhibition of trans-translation. These findings provide an important proof-of-concept that trans-translation is a promising antitubercular drug target.

microbiology↗

bioRxiv2024

Thiol Stress Fuels Pyrazinamide Action Against Mycobacterium tuberculosis

Pyrazinamide (PZA) is a cornerstone of first-line antitubercular drug therapy and is unique in its ability to kill nongrowing populations of Mycobacterium tuberculosis through disruption of coenzyme A synthesis. Unlike other drugs, PZA action is conditional and requires potentiation by host-relevant environmental stressors, such as low pH and nutrient limitation. Despite its pivotal role in tuberculosis therapy, the durability of this crucial drug is challenged by the emergent spread of drug-resistance. To advance drug discovery efforts, we characterized the activity of a more potent PZA analog, morphazinamide (MZA). Here, we demonstrate that like PZA, MZA acts in part through impairment of coenzyme A synthesis. Unexpectedly, we find that, in contrast to PZA, MZA does not require potentiation and maintains bactericidal activity against PZA-resistant strains due to an additional mechanism involving aldehyde release. Further, we find that the principal mechanism for resistance to the aldehyde component is through promoter mutations that increase expression of the mycothiol oxidoreductase MscR. Our findings reveal a dual action synergistic mechanism of MZA that results in a faster kill rate and a higher barrier to resistance. These observations provide new insights for discovery of improved therapeutic approaches for addressing the growing problem of drug-resistant tuberculosis. Significance StatementPyrazinamide is the only antitubercular drug of its kind, capable of targeting persistent Mycobacterium tuberculosis through disruption of the coenzyme A biosynthetic pathway. With the emergent spread of drug-resistant tuberculosis, it is imperative to identify more effective next-generation drugs. In this study, we characterized the mechanism of action of a more potent analog of pyrazinamide, morphazinamide. We demonstrate that like pyrazinamide, morphazinamide impairs coenzyme A metabolism. In contrast to pyrazinamide, we find that morphazinamide has an additional aldehyde-dependent mechanism that mediates potent bactericidal activity against both pyrazinamide-susceptible and pyrazinamide-resistant strains of M. tuberculosis. These findings open up new opportunities for the development of next-generation antitubercular drugs to tackle the increasing challenge of drug-resistant tuberculosis.

microbiology↗

bioRxiv2024

A biodegradable and restorative peripheral neural interface for the interrogation of neuropathic injuries

Monitoring the early-stage healing of severe traumatic nerve injuries is essential to gather physiological and pathological information for timely interventions and optimal clinical outcomes. While implantable peripheral nerve interfaces provide direct access to nerve fibers for precise interrogation and modulation, conventional non-degradable designs pose limited utilization in nerve injury rehabilitation. Here, we introduce a biodegradable and restorative neural interface for wireless real-time tracking and recovery of long-gap nerve injuries. Leveraging machine learning techniques, this electronic platform deciphers nerve recovery status and identifies traumatic neuroma formation at the early phase, enabling timely intervention and significantly improved therapeutic outcomes. The biodegradable nature of the device eliminates the need for retrieval procedures, reducing infection risks and secondary tissue damage. This research sheds light on bioresorbable multifunctional peripheral nerve interfaces for probing neuropathic injuries, offering vital information for early diagnosis and therapeutic intervention.

bioengineering↗

bioRxiv2024

MitoStructSeg: A Comprehensive Platform for Mitochondrial Structure Segmentation and Analysis

Mitochondrial morphology and structural changes are closely associated with metabolic dysfunction and disease progression. However, the structural complexity of mitochondria presents a major challenge for accurate segmentation and analysis. Most existing methods focus on delineating entire mitochondria but lack the capability to resolve fine internal features, particularly cristae. In this study, we introduce MitoStructSeg, a deep learning-based framework for mitochondrial structure segmentation and quantitative analysis. The core of MitoStructSeg is AMM-Seg, a novel model that integrates domain adaptation to improve cross-sample generalization, dual-channel feature fusion to enhance structural detail extraction, and continuity learning to preserve spatial coherence. This architecture enables accurate segmentation of both mitochondrial membranes and intricately folded cristae. MitoStructSeg further incorporates a quantitative analysis module that extracts key morphological metrics, including surface area, volume, and cristae density, allowing comprehensive and scalable assessment of mitochondrial morphology. The effectiveness of our approach has been validated on both human myocardial tissue and mouse kidney tissue, demonstrating its robustness in accurately segmenting mitochondria with diverse morphologies. In addition, we provide an open source, user-friendly tool to ensure practical usability.

bioinformatics↗