Microbial influence in Spanish bentonite slurry microcosms: Unveiling a-year long geochemical evolution and early-stage copper corrosion related to nuclear waste repositories.

The deep geological repository (DGR) concept consists of storing radioactive waste in metal canisters, surrounded by compacted bentonite, and placed deeply into a geological formation. Here, bentonite slurry microcosms with copper canisters, inoculated with bacterial consortium and amended with acetate, lactate and sulfate were set up to investigate their geochemical evolution over a year under anoxic conditions. The impact of microbial communities on the corrosion of the copper canisters in an early-stage (45 days) was also assessed. The amended bacterial consortium and electron donors/acceptor accelerated the microbial activity, while the heat-shocked process had a retarding effect. The microbial communities partially oxidize lactate to acetate, which is subsequently consumed when the lactate is depleted. Early-stage microbial communities showed that the bacterial consortium reduced microbial diversity with Pseudomonas and Stenotrophomonas dominating the community. However, sulfate-reducing bacteria such as Desulfocurvibacter, Anaerosolibacter, and Desulfosporosinus were enriched coupling oxidation of lactate/acetate with reduction of sulfates. The generated biogenic sulfides, which could mediate the conversion of copper oxides (possibly formed by trapped oxygen molecules on the bentonite or driven by the reduction of H2O) to copper sulfide (Cu2S), were identified by X-ray photoelectron spectroscopy (XPS). Overall, these findings shed light on the ideal geochemical conditions that would affect the stability of DGR barriers, emphasizing the impact of the SRB on the corrosion of the metal canisters, the gas generation, and the interaction with components of the bentonite.

Faecal proteomics links neutrophil degranulation with mortality in patients with alcohol-associated hepatitis.

OBJECTIVE: Patients with alcohol-associated hepatitis (AH) have a high mortality. Alcohol exacerbates liver damage by inducing gut dysbiosis, bacterial translocation and inflammation, which is characterised by increased numbers of circulating and hepatic neutrophils. DESIGN: In this study, we performed tandem mass tag (TMT) proteomics to analyse proteins in the faeces of controls (n=19), patients with alcohol-use disorder (AUD; n=20) and AH (n=80) from a multicentre cohort (InTeam). To identify protein groups that are disproportionately represented, we conducted over-representation analysis using Reactome pathway analysis and Gene Ontology to determine the proteins with the most significant impact. A faecal biomarker and its prognostic effect were validated by ELISA in faecal samples from patients with AH (n=70), who were recruited in a second and independent multicentre cohort (AlcHepNet). RESULT: Faecal proteomic profiles were overall significantly different between controls, patients with AUD and AH (principal component analysis p=0.001, dissimilarity index calculated by the method of Bray-Curtis). Proteins that showed notable differences across all three groups and displayed a progressive increase in accordance with the severity of alcohol-associated liver disease were predominantly those located in neutrophil granules. Over-representation and Reactome analyses confirmed that differentially regulated proteins are part of granules in neutrophils and the neutrophil degranulation pathway. Myeloperoxidase (MPO), the marker protein of neutrophil granules, correlates with disease severity and predicts 60-day mortality. Using an independent validation cohort, we confirmed that faecal MPO levels can predict short-term survival at 60 days. CONCLUSIONS: We found an increased abundance of faecal proteins linked to neutrophil degranulation in patients with AH, which is predictive of short-term survival and could serve as a prognostic non-invasive marker.

Nuclear Quantum Effects on the Electronic Structure of Water and Ice.

The electronic properties and optical response of ice and water are intricately shaped by their molecular structure, including the quantum mechanical nature of the hydrogen atoms. Despite numerous previous studies, a comprehensive understanding of the nuclear quantum effects (NQEs) on the electronic structure of water and ice at finite temperatures remains elusive. Here, we utilize molecular simulations that harness efficient machine-learning potentials and many-body perturbation theory to assess how NQEs impact the electronic bands of water and hexagonal ice. By comparing path-integral and classical simulations, we find that NQEs lead to a larger renormalization of the fundamental gap of ice, compared to that of water, ultimately yielding similar bandgaps in the two systems, consistent with experimental estimates. Our calculations suggest that the increased quantum mechanical delocalization of protons in ice, relative to water, is a key factor leading to the enhancement of NQEs on the electronic structure of ice.

Long-term tracking of the microbiology of uranium-amended water-saturated bentonite microcosms: A mechanistic characterization of U speciation.

Deep geological repositories (DGRs) stand out as one of the optimal options for managing high-level radioactive waste (HLW) such as uranium (U) in the near future. Here, we provide novel insights into microbial behavior in the DGR bentonite barrier, addressing potential worst-case scenarios such as waste leakage (e.g., U) and groundwater infiltration of electron rich donors in the bentonite. After a three-year anaerobic incubation, Illumina sequencing results revealed a bacterial diversity dominated by anaerobic and spore-forming microorganisms mainly from the phylum Firmicutes. Highly U tolerant and viable bacterial isolates from the genera Peribacillus, Bacillus, and some SRB such as Desulfovibrio and Desulfosporosinus, were enriched from U-amended bentonite. The results obtained by XPS and XRD showed that U was present as U(VI) and as U(IV) species. Regarding U(VI), we have identified biogenic U(VI) phosphates, U(UO2)·(PO4)2, located in the inner part of the bacterial cell membranes in addition to U(VI)-adsorbed to clays such as montmorillonite. Biogenic U(IV) species as uraninite may be produced as result of bacterial enzymatic U(VI) reduction. These findings suggest that under electron donor-rich water-saturation conditions, bentonite microbial community can control U speciation, immobilizing it, and thus enhancing future DGR safety if container rupture and waste leakage occurs.

Confinement Effects on Proton Transfer in TiO2 Nanopores from Machine Learning Potential Molecular Dynamics Simulations.

Improved understanding of proton transfer in nanopores is critical for a wide range of emerging applications, yet experimentally probing mechanisms and energetics of this process remains a significant challenge. To help reveal details of this process, we developed and applied a machine learning potential derived from first-principles calculations to examine water reactivity and proton transfer in TiO2 slit-pores. We find that confinement of water within pores smaller than 0.5 nm imposes strong and complex effects on water reactivity and proton transfer. Although the proton transfer mechanism is similar to that at a TiO2 interface with bulk water, confinement reduces the activation energy of this process, leading to more frequent proton transfer events. This enhanced proton transfer stems from the contraction of oxygen-oxygen distances dictated by the interplay between confinement and hydrophilic interactions. Our simulations also highlight the importance of the surface topology, where faster proton transport is found in the direction where a unique arrangement of surface oxygens enables the formation of an ordered water chain. In a broader context, our study demonstrates that proton transfer in hydrophilic nanopores can be enhanced by controlling pore size, surface chemistry, and topology.

Liraglutide Pretreatment Does Not Improve Acute Doxorubicin-Induced Cardiotoxicity in Rats.

Doxorubicin is an effective drug for cancer treatment; however, cardiotoxicity limits its use. Cardiotoxicity pathophysiology is multifactorial. GLP-1 analogues have been shown to reduce oxidative stress and inflammation. In this study, we evaluated the effect of pretreatment with liraglutide on doxorubicin-induced acute cardiotoxicity. A total of 60 male Wistar rats were allocated into four groups: Control (C), Doxorubicin (D), Liraglutide (L), and Doxorubicin + Liraglutide (DL). L and DL received subcutaneous injection of liraglutide 0.6 mg/kg daily, while C and D received saline for 2 weeks. Afterwards, D and DL received a single intraperitoneal injection of doxorubicin 20 mg/kg; C and L received an injection of saline. Forty-eight hours after doxorubicin administration, the rats were subjected to echocardiogram, isolated heart functional study, and euthanasia. Liraglutide-treated rats ingested significantly less food and gained less body weight than animals that did not receive the drug. Rats lost weight after doxorubicin injection. At echocardiogram and isolated heart study, doxorubicin-treated rats had systolic and diastolic function impairment. Myocardial catalase activity was statistically higher in doxorubicin-treated rats. Myocardial protein expression of tumor necrosis factor alpha (TNF-α), phosphorylated nuclear factor-κB (p-NFκB), troponin T, and B-cell lymphoma 2 (Bcl-2) was significantly lower, and the total NFκB/p-NFκB ratio and TLR-4 higher in doxorubicin-treated rats. Myocardial expression of OPA-1, MFN-2, DRP-1, and topoisomerase 2ß did not differ between groups (p > 0.05). In conclusion, doxorubicin-induced cardiotoxicity is accompanied by decreased Bcl-2 and phosphorylated NFκB and increased catalase activity and TLR-4 expression. Liraglutide failed to improve acute doxorubicin-induced cardiotoxicity in rats.

The lipopolysaccharide-TLR4 axis regulates hepatic glutaminase 1 expression promoting liver ammonia build-up as steatotic liver disease progresses to steatohepatitis.

INTRODUCTION: Ammonia is a pathogenic factor implicated in the progression of metabolic-associated steatotic liver disease (MASLD). The contribution of the glutaminase 1 (GLS) isoform, an enzyme converting glutamine to glutamate and ammonia, to hepatic ammonia build-up and the mechanisms underlying its upregulation in metabolic-associated steatohepatitis (MASH) remain elusive. METHODS: Multiplex transcriptomics and targeted metabolomics analysis of liver biopsies in dietary mouse models representing the whole spectra of MASLD were carried out to characterize the relevance of hepatic GLS during disease pathological progression. In addition, the acute effect of liver-specific GLS inhibition in hepatic ammonia content was evaluated in cultured hepatocytes and in in vivo mouse models of diet-induced MASLD. Finally, the regulatory mechanisms of hepatic GLS overexpression related to the lipopolysaccharide (LPS)/Toll-like receptor 4 (TLR4) axis were explored in the context of MASH. RESULTS: In mouse models of diet-induced MASLD, we found that augmented liver GLS expression is closely associated with the build-up of hepatic ammonia as the disease progresses from steatosis to steatohepatitis. Importantly, the acute silencing/pharmacological inhibition of GLS diminishes the ammonia burden in cultured primary mouse hepatocytes undergoing dedifferentiation, in steatotic hepatocytes, and in a mouse model of diet-induced steatohepatitis, irrespective of changes in ureagenesis and gut permeability. Under these conditions, GLS upregulation in the liver correlates positively with the hepatic expression of TLR4 that recognizes LPS. In agreement, the pharmacological inhibition of TLR4 reduces GLS and hepatic ammonia content in LPS-stimulated mouse hepatocytes and hyperammonemia animal models of endotoxemia. CONCLUSIONS: Overall, our results suggest that the LPS/TLR4 axis regulates hepatic GLS expression promoting liver ammonia build-up as steatotic liver disease progresses to steatohepatitis.

Nonlinear Effects of Hydrophobic Confinement on the Electronic Structure and Dielectric Response of Water.

Fundamental studies of the dielectrics of confined water are critical to understand the ion transport across biological and synthetic nanochannels. The relevance of these fundamental studies, however, surmounts the difficulty of probing water's dielectric constant as a function of a fine variation in confinement. In this work, we explore the computational efficiency of machine learning potentials to derive the confinement effects on the dielectric constant, polarization, and dipole moment of water. Our simulations predict an enhancement of the axial dielectric constant of water under extreme confinement, arising from either the formation of ferroelectric structures of ordered water or larger dipole fluctuations facilitated by the disruption of water's H-bond network. Our study highlights the impact of hydrophobic nanoconfinement on the dielectric constant and on the ionic and electronic structure of water molecules, pointing to the importance of geometric flexibility and electronic polarizability to properly model confinement effects on water.

Mitochondrial antiviral signaling protein enhances MASLD progression through the ERK/TNFα/NFκß pathway.

BACKGROUND AND AIMS: Mitochondrial antiviral signaling protein (MAVS) is a critical regulator that activates the host's innate immunity against RNA viruses, and its signaling pathway has been linked to the secretion of proinflammatory cytokines. However, the actions of MAVS on inflammatory pathways during the development of metabolic dysfunction-associated steatotic liver disease (MASLD) have been little studied. APPROACH AND RESULTS: Liver proteomic analysis of mice with genetically manipulated hepatic p63, a transcription factor that induces liver steatosis, revealed MAVS as a target downstream of p63. MAVS was thus further evaluated in liver samples from patients and in animal models with MASLD. Genetic inhibition of MAVS was performed in hepatocyte cell lines, primary hepatocytes, spheroids, and mice. MAVS expression is induced in the liver of both animal models and people with MASLD as compared with those without liver disease. Using genetic knockdown of MAVS in adult mice ameliorates diet-induced MASLD. In vitro, silencing MAVS blunts oleic and palmitic acid-induced lipid content, while its overexpression increases the lipid load in hepatocytes. Inhibiting hepatic MAVS reduces circulating levels of the proinflammatory cytokine TNFα and the hepatic expression of both TNFα and NFκß. Moreover, the inhibition of ERK abolished the activation of TNFα induced by MAVS. The posttranslational modification O -GlcNAcylation of MAVS is required to activate inflammation and to promote the high lipid content in hepatocytes. CONCLUSIONS: MAVS is involved in the development of steatosis, and its inhibition in previously damaged hepatocytes can ameliorate MASLD.

Inhibition of hepatic p63 ameliorates steatohepatitis with fibrosis in mice.

OBJECTIVE: p63 is a transcription factor involved in multiple biological functions. In the liver, the TAp63 isoform induces lipid accumulation in hepatocytes. However, the role of liver TAp63 in the progression of metabolic dysfunction-associated steatohepatitis (MASH) with fibrosis is unknown. METHODS: We evaluated the hepatic p63 levels in different mouse models of steatohepatitis with fibrosis induced by diet. Next, we used virogenetic approaches to manipulate the expression of TAp63 in adult mice under diet-induced steatohepatitis with fibrosis and characterized the disease condition. Finally, we performed proteomics analysis in mice with overexpression and knockdown of hepatic TAp63. RESULTS: Levels of TAp63, but not of ΔN isoform, are increased in the liver of mice with diet-induced steatohepatitis with fibrosis. Both preventive and interventional strategies for the knockdown of hepatic TAp63 significantly ameliorated diet-induced steatohepatitis with fibrosis in mice fed a methionine- and choline-deficient diet (MCDD) and choline deficient and high fat diet (CDHFD). The overexpression of hepatic TAp63 in mice aggravated the liver condition in mice fed a CDHFD. Proteomic analysis in the liver of these mice revealed alteration in multiple proteins and pathways, such as oxidative phosphorylation, antioxidant activity, peroxisome function and LDL clearance. CONCLUSIONS: These results indicate that liver TAp63 plays a critical role in the progression of diet-induced steatohepatitis with fibrosis, and its inhibition ameliorates the disease.

Impaired oxygenation after lung resection: Incidence and perioperative risk factors.

STUDY OBJECTIVE: To estimate the incidence of postoperative oxygenation impairment after lung resection in the era of lung-protective management, and to identify perioperative factors associated with that impairment. DESIGN: Registry-based retrospective cohort study. SETTING: Two large academic hospitals in the United States. PATIENTS: 3081 ASA I-IV patients undergoing lung resection. MEASUREMENTS: 79 pre- and intraoperative variables, selected for inclusion based on a causal inference framework. The primary outcome of impaired oxygenation, an early marker of lung injury, was defined as at least one of the following within seven postoperative days: (1) SpO2 < 92%; (2) imputed PaO2/FiO2 < 300 mmHg [(1) or (2) occurring at least twice within 24 h]; (3) intensive oxygen therapy (mechanical ventilation or > 50% oxygen or high-flow oxygen). MAIN RESULTS: Oxygenation was impaired within seven postoperative days in 70.8% of patients (26.6% with PaO2/FiO2 < 200 mmHg or intensive oxygen therapy). In multivariable analysis, each additional cmH2O of intraoperative median driving pressure was associated with a 7% higher risk of impaired oxygenation (OR 1.07; 95%CI 1.04 to 1.10). Higher median intraoperative FiO2 (OR 1.23; 95%CI 1.14 to 1.31 per 0.1) and PEEP (OR 1.12; 95%CI 1.04 to 1.21 per 1 cm H2O) were also associated with increased risk. History of COPD (OR 2.55; 95%CI 1.95 to 3.35) and intraoperative albuterol administration (OR 2.07; 95%CI 1.17 to 3.67) also showed reliable effects. CONCLUSIONS: Impaired postoperative oxygenation is common after lung resection and is associated with potentially modifiable pre- and intraoperative respiratory factors.

Insights into the Impact of Physicochemical and Microbiological Parameters on the Safety Performance of Deep Geological Repositories.

Currently, the production of radioactive waste from nuclear industries is increasing, leading to the development of reliable containment strategies. The deep geological repository (DGR) concept has emerged as a suitable storage solution, involving the underground emplacement of nuclear waste within stable geological formations. Bentonite clay, known for its exceptional properties, serves as a critical artificial barrier in the DGR system. Recent studies have suggested the stability of bentonite within DGR relevant conditions, indicating its potential to enhance the long-term safety performance of the repository. On the other hand, due to its high resistance to corrosion, copper is one of the most studied reference materials for canisters. This review provides a comprehensive perspective on the influence of nuclear waste conditions on the characteristics and properties of DGR engineered barriers. This paper outlines how evolving physico-chemical parameters (e.g., temperature, radiation) in a nuclear repository may impact these barriers over the lifespan of a repository and emphasizes the significance of understanding the impact of microbial processes, especially in the event of radionuclide leakage (e.g., U, Se) or canister corrosion. Therefore, this review aims to address the long-term safety of future DGRs, which is critical given the complexity of such future systems.

Pannexin 1 dysregulation in Duchenne muscular dystrophy and its exacerbation of dystrophic features in mdx mice.

BACKGROUND: Duchenne muscular dystrophy (DMD) is associated with impaired muscle regeneration, progressive muscle weakness, damage, and wasting. While the cause of DMD is an X-linked loss of function mutation in the gene encoding dystrophin, the exact mechanisms that perpetuate the disease progression are unknown. Our laboratory has demonstrated that pannexin 1 (Panx1 in rodents; PANX1 in humans) is critical for the development, strength, and regeneration of male skeletal muscle. In normal skeletal muscle, Panx1 is part of a multiprotein complex with dystrophin. We and others have previously shown that Panx1 levels and channel activity are dysregulated in various mouse models of DMD. METHODS: We utilized myoblast cell lines derived from DMD patients to assess PANX1 expression and function. To investigate how Panx1 dysregulation contributes to DMD, we generated a dystrophic (mdx) mouse model that lacks Panx1 (Panx1-/-/mdx). In depth characterization of this model included histological analysis, as well as locomotor, and physiological tests such as muscle force and grip strength assessments. RESULTS: Here, we demonstrate that PANX1 levels and channel function are reduced in patient-derived DMD myoblast cell lines. Panx1-/-/mdx mice have a significantly reduced lifespan, and decreased body weight due to lean mass loss. Their tibialis anterior were more affected than their soleus muscles and displayed reduced mass, myofiber loss, increased centrally nucleated myofibers, and a lower number of muscle stem cells compared to that of Panx1+/+/mdx mice. These detrimental effects were associated with muscle and locomotor functional impairments. In vitro, PANX1 overexpression in patient-derived DMD myoblasts improved their differentiation and fusion. CONCLUSIONS: Collectively, our findings suggest that PANX1/Panx1 dysregulation in DMD exacerbates several aspects of the disease. Moreover, our results suggest a potential therapeutic benefit to increasing PANX1 levels in dystrophic muscles.

Prevalence of Concomitant Distal Suprascapular Nerve Injury in Patients with Root-level Brachial Plexus Palsy: A Clinical Anatomic Study of Injury Pattern.

BACKGROUND: Root-level suprascapular nerve palsy is commonly reconstructed via spinal accessory nerve transfer in brachial plexus injury, yet some patients fail to recover. We hypothesize that this relates to concomitant undetected lesions distal to the nerve transfer coaptation. METHODS: 67 patients with plexus injury and C5/6 root involvement were included in this prospective study between March 2021 and October 2022. During spinal accessory to suprascapular nerve transfer the entire suprascapular nerve was explored, via cresenteric clavicular osteotomy, and anatomic variations and injury patterns categorized. RESULTS: Proximal root involvement was C5-C6 (n=8), C5-C7 (n=13), C5-C8 (n=17), C5-T1(29). Mean time from injury to surgery was 5.6 months. The suprascapular nerve was found to be injured in 16/67 cases (24%). In 9 cases (13%) the lesion was proximal to the suprascapular fossa. In 3 cases (4%) the suprascapular nerve was injured both proximally and within the fossa, and in 4 cases (6%) in the fossa or distal to it. Therefore, in 7 cases (10%), a traditional suprascapular nerve transfer would not successfully bypass the zone of injury of the suprascapular nerve in the fossa. Of the 16 cases of concomitant suprascapular nerve injury, 1/8 in occurred in C5-C6 root injury, 4/13 of C5-C7 root injury, 5/17 of C5-C8 root injury and 6/39 in total paralysis. CONCLUSIONS: Concomitant distal suprascapular nerve injury in brachial plexus stretch palsy occurred in 24% of the cases. This warrants attention from the surgeon to identify distal lesions and to perform the nerve transfer beyond any secondary lesions.

Regional pulmonary perfusion, blood volume, and their relationship change in experimental early ARDS.

Regional pulmonary perfusion (Q) has been investigated using blood volume (Fb) imaging as an easier-to-measure surrogate. However, it is unclear if changing pulmonary conditions could affect their relationship. We hypothesized that vascular changes in early acute respiratory distress syndrome (ARDS) affect Q and Fb differently. Five sheep were anesthetized and received lung protective mechanical ventilation for 20 h while endotoxin was continuously infused. Using dynamic 18F-FDG and 13NN Positron Emission Tomography (PET), regional Fb and Q were analysed in 30 regions of interest (ROIs) and normalized by tissue content (Fbn and Qn, respectively). After 20 h, the lung injury showed characteristics of early ARDS, including gas exchange and lung mechanics. PET images of Fbn and Qn showed substantial differences between baseline and lung injury. Lung injury caused a significant change in the Fbn-Qn relationship compared to baseline (p < 0.001). The best models at baseline and lung injury were Fbn = 0.32 + 0.690Qn and Fbn = 1.684Qn-0.538Qn2, respectively. Endotoxine-associated early ARDS changed the relationship between Fb and Q, shifting from linear to curvilinear. Effects of endotoxin exposure on the vasoactive blood flow regulation were most likely the key factor for this change limiting the quantitative accuracy of Fb imaging as a surrogate for regional Q.

p63 controls metabolic activation of hepatic stellate cells and fibrosis via an HER2-ACC1 pathway.

The p63 protein has pleiotropic functions and, in the liver, participates in the progression of nonalcoholic fatty liver disease (NAFLD). However, its functions in hepatic stellate cells (HSCs) have not yet been explored. TAp63 is induced in HSCs from animal models and patients with liver fibrosis and its levels positively correlate with NAFLD activity score and fibrosis stage. In mice, genetic depletion of TAp63 in HSCs reduces the diet-induced liver fibrosis. In vitro silencing of p63 blunts TGF-ß1-induced HSCs activation by reducing mitochondrial respiration and glycolysis, as well as decreasing acetyl CoA carboxylase 1 (ACC1). Ectopic expression of TAp63 induces the activation of HSCs and increases the expression and activity of ACC1 by promoting the transcriptional activity of HER2. Genetic inhibition of both HER2 and ACC1 blunt TAp63-induced activation of HSCs. Thus, TAp63 induces HSC activation by stimulating the HER2-ACC1 axis and participates in the development of liver fibrosis.

Changing Clinical Epidemiology of Plasmodium vivax Malaria as Transmission Decreases: Population-Based Prospective Panel Survey in the Brazilian Amazon.

BACKGROUND: Malarial infections are often missed by microscopy, and most parasite carriers are asymptomatic in low-endemicity settings. Whether parasite detectability and its ability to elicit symptoms change as transmission declines remains unclear. METHODS: We performed a prospective panel survey with repeated measurements on the same participants over 12 months to investigate whether Plasmodium vivax detectability by microscopy and risk of symptoms upon infection varied during a community-wide larviciding intervention in the Amazon basin of Brazil that markedly reduced vector density. We screened 1096 to 1400 residents in the intervention site for malaria by microscopy and quantitative TaqMan assays at baseline and twice during intervention. RESULTS: We found that more P vivax infections than expected from their parasite densities measured by TaqMan assays were missed by microscopy as transmission decreased. At lower transmission, study participants appeared to tolerate higher P vivax loads without developing symptoms. We hypothesize that changes in the ratio between circulating parasites and those that accumulate in the bone marrow and spleen, by avoiding peripheral blood microscopy detection, account for decreased parasite detectability and lower risk of symptoms under low transmission. CONCLUSIONS: P vivax infections are more likely to be subpatent and remain asymptomatic as malaria transmission decreases.

Non-animal protein hydrolysates from agro-industrial wastes: A prospect of alternative inputs for cultured meat.

In light of the growing demand for alternative protein sources, laboratory-grown meat has been proposed as a potential solution to the challenges posed by conventional meat production. Cultured meat does not require animal slaughter and uses sustainable production methods, contributing to animal welfare, human health, and environmental sustainability. However, some challenges still need to be addressed in cultured meat production, such as the use of fetal bovine serum for medium supplementation. This ingredient has limited availability, increases production costs, and raises ethical concerns. This review explores the potential of non-animal protein hydrolysates derived from agro-industrial wastes as substitutes for critical components of fetal bovine serum in cultured meat production. Despite the lack of standardization of hydrolysate composition, the potential benefits of this alternative protein source may outweigh its disadvantages. Future research holds promise for increasing the accessibility of cultured meat.