Several years after its emergence, coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [ 1, 2], has evolved into a persistent and complex public health issue [ 3]. Although widespread vaccination [ 4, 5] and antiviral therapies [ 6] have significantly reduced mortality, SARS-CoV-2 continues to circulate and evolve, producing variants with altered transmissibility and immune escape potential [ 7]. Thus, although initially considered a viral pneumonia with occasional extrapulmonary complications, COVID-19 is now recognized as a complex disorder in which viral persistence, immune dysregulation, endothelial injury, and autoimmunity intersect in significant clinical ways [ 8, 9]. As a result, scientific research has moved from an emergency response toward a deeper understanding of viral biology, host interactions, and innovative therapeutic strategies. The papers collected in this Special Issue contribute to a growing body of evidence showing that SARS-CoV-2 can provoke not only acute inflammation but also sustain immunological alterations that may persist well beyond the infectious phase [ 10, 11]. A key step in SARS-CoV-2 infection is the interaction between the viral spike protein and the Angiotensin-Converting Enzyme 2 (ACE2) receptor on host cells [ 12]. Biskupek and Gieldon (Contribution 1) propose a two-stage recognition mechanism in which viral attachment involves a transient intermediate state between the receptor-binding domain and ACE2. Their research identified critical residues (R403, Y501, and F486) that contribute to this dynamic interaction. This model challenges the traditional view of a simple lock-and-key binding and instead describes viral entry as a dynamic multi-step process. This point of view could explain how mutations in emerging variants can modulate infectivity without necessarily increasing binding affinity. Importantly, it also suggests new therapeutic strategies targeting intermediate conformational states to eliminate the infection. The study by Nukaga et al. (Contribution 2) introduces a new mechanism of viral-host interaction. They identified a SARS-CoV-2–derived RNA fragment capable of suppressing the human ATP5A gene via a siRNA-like mechanism leading to ATP depletion, oxidative stress, and impaired cellular maturation in cardiomyocytes, suggesting that viral RNA itself may act as a regulatory molecule within host cells. Moreover, these effects occur independently of direct viral infection, supporting the hypothesis that circulating viral RNA fragments can mediate distal organ injury such as myocardial injury [ 13, 14]. Complementing this molecular mechanism, the study by Pius-Sadowska et al. (Contribution 3) highlights the central role of vascular dysfunction in severe COVID-19 [ 15]. Their findings highlight an imbalance between procoagulant and regulatory factors, particularly the vWF/ADAMTS13 axis, along with elevated VEGFR and reduced DPP-IV levels as predictors of ICU admission. These alterations suggest a state of endothelial activation, impaired angiogenesis, and nitric oxide deficiency, all of which contribute to a hypercoagulable environment. In agreement with these findings, we previously found a significant increase in serum anti-neutrophil cytoplasmic antibody (ANCA) levels in hospitalized COVID-19 patients compared to both controls and asymptomatic patients, and this increase was associated with disease severity. However, the ANCA increase was transient and none of the patients had clinical signs of ANCA-associated vasculitis except for a severe pulmonary involvement [ 16]. Among innovative therapeutic strategies, Asiedu et al. (Contribution 4) proposed an alternative host-targeted antiviral strategy based on mycolactone (MLN), a multitarget compound capable of interfering with SARS-CoV-2 infection [ 17]. They found that MLN leads to viral inhibition at nanomolar concentrations, therefore with a more effective action than antivirals such as remdesivir, and also versus multiple variants, including Alpha, Delta, and Omicron. MLN acts by disrupting clathrin-mediated endocytosis and viral fusion processes blocking both viral entry and intracellular spread. Therefore, this host-targeted approach may reduce the likelihood of resistance resulting from viral mutations. In addition to viral entry and pharmacological interventions, the host response plays a central role in determining disease progression and clinical outcomes. Milicevic et al. (Contribution 5) describe the results obtained through transcriptomic analyses of paired nasopharyngeal swabs and blood samples collected during the acute and resolved phases of infection. Their study reveals a broad upregulation of immunity-related genes, particularly those associated with interferon signaling, along with significant alterations in hundreds of biological pathways. In agreement with these findings, we found variants in genes related to autoimmune and/or autoinflammatory diseases in about 83% of children with multisystem inflammatory syndrome, a rare severe complication of COVID-19 [ 18]. Ravindran et al. (Contribution 6) applied a lipidomic approach coupled with multiplex analysis to characterized lipid mediators [ 19] and chemokines profiles in COVID-19 patients. They found significantly increased levels of pro-inflammatory cytokines/chemokines in patients with severe disease, while anti-inflammatory lipid mediators were significantly elevated in patients with a mild phenotype. Interestingly, the increase in lipid mediators occurs earlier than cytokines, inducing anti-inflammatory mechanisms. Finally, Yendo et al. (Contribution 7) studied the antiviral immune response in the skin, focusing on type I interferons (IFNs). Their results showed a compartmentalized immune response. In fact, IFN-β expression was increased in the epidermis, while reduced in the dermis, together with reduced expression of key signaling molecules such as STING and TLR7. This suggests that SARS-CoV-2 may differentially modulate innate immunity depending on the tissue, which could likely allow viral persistence in certain tissues. The presence of viral particles and microvascular thrombi in skin tissues further links local immune responses to systemic vascular pathology. It is noteworthy that, despite systemic hyperinflammation, skin manifestations remain relatively mild, likely reflecting a partially effective but tightly regulated interferon response. In agreement with these findings, no significant correlation was found between skin manifestations and disease severity in a single-center observational study in Italy [ 20]. The studies presented here collectively reinforce the idea that COVID-19 should be understood as a systemic immunovascular disorder whose consequences may extend far beyond the acute phase of infection [ 16, 18] (Contribution 7), reminding the scientific community that SARS-CoV-2 is not simply a respiratory virus. It is an immunological stress test capable of revealing hidden vulnerabilities in host defense, vascular biology, and immune tolerance [ 8, 21]. In conclusion, COVID-19 continues to serve as a model for modern infectious disease research. While significant progress has been made, future efforts should focus on translating molecular knowledge into effective clinical interventions, developing therapies that can resist viral evolution, and managing the long-term consequences of infection. A deeper understanding of the interaction between SARS-CoV-2 and the host will remain essential not only for managing COVID-19 but also for preparing for future emerging infectious diseases. References Cevik, M.; Bamford, C.G.G.; Ho, A. COVID-19 pandemic-a focused review for clinicians. Clin. Microbiol. Infect. 2020, 26, 842–847. [] [ CrossRef] [ PubMed] Chen, Y.; Liu, Q.; Guo, D. Emerging coronaviruses: Genome structure, replication, and pathogenesis. J. Med. Virol. 2020, 92, 418–423, Correction in J. Med. Virol. 2020, 92, 2249. [] [ CrossRef] [ PubMed] WHO. Six Years After COVID-19’s Global Alarm: Is the World Better Prepared for the Next Pandemic? Available online: https://www.who.int/ (accessed on 17 April 2026). Sithole, M.N.; Khan, M.R.; Mohammed, H.A.; Khan, R.A.; Naik, K.; Choonara, Y.E. A systematic review on vaccine developmental approaches: Evaluating efficacy, and addressing challenges of infectious diseases in the post-COVID-19 era. Virus Res. 2026, 367, 199720. [] [ CrossRef] [ PubMed] Cortese, P.; Amato, F.; Davino, A.; De Franchis, R.; Esposito, S.; Zollo, I.; Di Domenico, M.; Solito, E.; Zarrilli, F.; Gentile, L.; et al. The Immune Response to SARS-CoV-2 Vaccine in a Cohort of Family Pediatricians from Southern Italy. Cells 2023, 12, 1447. [] [ CrossRef] [ PubMed] Brüssow, H. Antivirals Targeting Coronavirus RNA-Dependent RNA Polymerase and Main Protease: From Mechanisms of Action to Outcomes in COVID-19 Clinical Trials. Microb. Biotechnol. 2026, 19, e70342. [] [ CrossRef] [ PubMed] Carabelli, A.M.; Peacock, T.P.; Thorne, L.G.; Harvey, W.T.; Hughes, J.; COVID-19 Genomics UK Consortium; Peacock, S.J.; Barclay, W.S.; de Silva, T.I.; Towers, G.J.; et al. SARS-CoV-2 variant biology: Immune escape, transmission and fitness. Nat. Rev. Microbiol. 2023, 21, 162–177. [] [ CrossRef] [ PubMed] Blanco-Melo, D.; Nilsson-Payant, B.E.; Liu, W.-C.; Uhl, S.; Hoagland, D.; Møller, R.; Jordan, T.X.; Oishi, K.; Panis, M.; Sachs, D.; et al. Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19. Cell 2020, 181, 1036–1045. [] [ CrossRef] [ PubMed] Hadjadj, J.; Yatim, N.; Barnabei, L.; Corneau, A.; Boussier, J.; Smith, N.; Péré, H.; Charbit, B.; Bondet, V.; Chenevier-Gobeaux, C.; et al. Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients. Science 2020, 369, 718–724. [] [ CrossRef] [ PubMed] Merad, M.; Martin, J.C. Pathological inflammation in patients with COVID-19: A key role for monocytes and macrophages. Nat. Rev. Immunol. 2020, 20, 355–362, Correction in Nat. Rev. Immunol. 2020, 20, 448. [] [ CrossRef] [ PubMed] Lucas, C.; Wong, P.; Klein, J.; Castro, T.B.R.; Silva, J.; Sundaram, M.; Ellingson, M.K.; Mao, T.; Oh, J.E.; Israelow, B.; et al. Longitudinal analyses reveal immunological misfiring in severe COVID-19. Nature 2020, 584, 463–469. [] [ CrossRef] [ PubMed] Lan, J.; Ge, J.; Yu, J.; Shan, S.; Zhou, H.; Fan, S.; Zhang, Q.; Shi, X.; Wang, Q.; Zhang, L.; et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature 2020, 581, 215–220. [] [ CrossRef] [ PubMed] Siddiqi, H.K.; Weber, B.; Zhou, G.; Regan, J.; Fajnzylber, J.; Coxen, K.; Corry, H.; Yu, X.G.; DiCarli, M.; Li, J.Z.; et al. Increased Prevalence of Myocardial Injury in Patients with SARS-CoV-2 Viremia. Am. J. Med. 2021, 134, 542–546. [] [ CrossRef] [ PubMed] Ferro, M.D.; Bussani, R.; Paldino, A.; Nuzzi, V.; Collesi, C.; Zentilin, L.; Schneider, E.; Correa, R.; Silvestri, F.; Zacchigna, S.; et al. SARS-CoV-2, myocardial injury and inflammation: Insights from a large clinical and autopsy study. Clin. Res. Cardiol. 2021, 110, 1822–1831, Correction in Clin. Res. Cardiol. 2021, 110, 1694. [] [ CrossRef] [ PubMed] Varga, Z.; Flammer, A.J.; Steiger, P.; Haberecker, M.; Andermatt, R.; Zinkernagel, A.S.; Mehra, M.R.; Schuepbach, R.A.; Ruschitzka, F.; Moch, H. Endothelial cell infection and endotheliitis in COVID-19. Lancet 2020, 395, 1417–1418. [] [ CrossRef] [ PubMed] Gelzo, M.; Cacciapuoti, S.; Pinchera, B.; De Rosa, A.; Cernera, G.; Scialò, F.; Comegna, M.; Mormile, M.; Gallicchio, A.; Fabbrocini, G.; et al. A Transient Increase in the Serum ANCAs in Patients with SARS-CoV-2 Infection: A Signal of Subclinical Vasculitis or an Epiphenomenon with No Clinical Manifestations? A Pilot Study. Viruses 2021, 13, 1718. [] [ CrossRef] [ PubMed] Ricci, D.; Demangel, C. From Bacterial Toxin to Therapeutic Agent: The Unexpected Fate of Mycolactone. Toxins 2023, 15, 369. [] [ CrossRef] [ PubMed] Gelzo, M.; Castaldo, A.; Giannattasio, A.; Scalia, G.; Raia, M.; Esposito, M.V.; Maglione, M.; Muzzica, S.; D’Anna, C.; Grieco, M.; et al. MIS-C: A COVID-19-associated condition between hypoimmunity and hyperimmunity. Front. Immunol. 2022, 13, 985433. [] [ CrossRef] [ PubMed] Serhan, C.N. Pro-resolving lipid mediators are leads for resolution physiology. Nature 2014, 510, 92–101. [] [ CrossRef] [ PubMed] Recalcati, S. Cutaneous manifestations in COVID-19: A first perspective. J. Eur. Acad. Dermatol. Venereol. 2020, 34, e212–e213. [] [ CrossRef] [ PubMed] McGonagle, D.; O’Donnell, J.S.; Sharif, K.; Emery, P.; Bridgewood, C. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia. Lancet Rheumatol. 2020, 2, e437–e445. [] [ CrossRef] [ PubMed] Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. Share and Cite Gelzo, M.; Amato, F.; Gentile, I.; Castaldo, G. Special Issue “Novel Approaches to Potential COVID-19 Molecular Therapeutics”. Int. J. Mol. Sci. 2026, 27, 5170. https://doi.org/10.3390/ijms27125170 Gelzo M, Amato F, Gentile I, Castaldo G. Special Issue “Novel Approaches to Potential COVID-19 Molecular Therapeutics”. International Journal of Molecular Sciences. 2026; 27(12):5170. https://doi.org/10.3390/ijms27125170 Gelzo, Monica, Felice Amato, Ivan Gentile, and Giuseppe Castaldo. 2026. "Special Issue “Novel Approaches to Potential COVID-19 Molecular Therapeutics”" International Journal of Molecular Sciences 27, no. 12: 5170. https://doi.org/10.3390/ijms27125170 Gelzo, M., Amato, F., Gentile, I., & Castaldo, G. (2026). Special Issue “Novel Approaches to Potential COVID-19 Molecular Therapeutics”. International Journal of Molecular Sciences, 27(12), 5170. https://doi.org/10.3390/ijms27125170 Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details . Article Metrics Article metric data becomes available approximately 24 hours after publication online. Conflicts of Interest The authors declare no conflicts of interest. Abbreviations The following abbreviations are used in this manuscript: COVID-19 Coronavirus disease 2019 SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 ACE2 Angiotensin-Converting Enzyme 2 ANCA Anti-neutrophil cytoplasmic antibody MLN Mycolactone List of Contributions Biskupek, I.; Gieldon, A. Two-Stage Recognition Mechanism of the SARS-CoV-2 Receptor-Binding Domain to Angiotensin-Converting Enzyme-2 (ACE2). Int. J. Mol. Sci. 2024, 25, 679. Nukaga, S.; Fujiwara-Tani, R.; Mori, T.; Kawahara, I.; Nishida, R.; Miyagawa, Y.; Goto, K.; Ohmori, H.; Fujii, K.; Sasaki, T.; et al. SARS-CoV-2-Derived RNA Fragment Induces Myocardial Dysfunction via siRNA-like Suppression of Mitochondrial ATP Synthase. Int. J. Mol. Sci. 2025, 26, 5392. Pius-Sadowska, E.; Kulig, P.; Niedźwiedź, A.; Baumert, B.; Łuczkowska, K.; Rogińska, D.; Sobuś, A.; Ulańczyk, Z.; Kawa, M.; Paczkowska, E.; et al. VEGFR and DPP-IV as Markers of Severe COVID-19 and Predictors of ICU Admission. Int. J. Mol. Sci. 2023, 24, 17003. Asiedu, S.O.; Gupta, Y.; Nicolaescu, V.; Gula, H.; Caulfield, T.R.; Durvasula, R.; Kempaiah, P.; Kwofie, S.K.; Wilson, M.D. Mycolactone: A Broad Spectrum Multitarget Antiviral Active in the Picomolar Range for COVID-19 Prevention and Cure. Int. J. Mol. Sci. 2023, 24, 7151. Milicevic, O.; Loncar, A.; Abazovic, D.; Vukcevic, M.; Despot, D.; Djukic, T.; Djukic, V.; Milovanovic, A.; Panic, N.; Plecic, N.; et al. Transcriptome from Paired Samples Improves the Power of Comprehensive COVID-19 Host-Viral Characterization. Int. J. Mol. Sci. 2023, 24, 13125. Ravindran, R.; O’connor, E.; Gupta, A.; Luciw, P.A.; Khan, A.I.; Dorreh, N.; Chiang, K.; Ikram, A.; Reddy, S. Lipid Mediators and Cytokines/Chemokines Display Differential Profiles in Severe versus Mild/Moderate COVID-19 Patients. Int. J. Mol. Sci. 2023, 24, 13054. Yendo, T.M.; Orfali, R.L.; Pereira, N.V.; Pereira, N.Z.; Ramos, Y.Á.L.; Kawakami, J.T.; Duarte-Neto, A.N.; Sotto, M.N.; Silva, L.F.F.; Duarte, A.J.d.S.; et al. Type I Interferons in SARS-CoV-2 Cutaneous Infection: Is There a Role in Antiviral Defense? Int. J. Mol. Sci. 2025, 26, 6049. References Cevik, M.; Bamford, C.G.G.; Ho, A. COVID-19 pandemic-a focused review for clinicians. Clin. Microbiol. Infect. 2020, 26, 842–847. [] [ CrossRef] [ PubMed] Chen, Y.; Liu, Q.; Guo, D. Emerging coronaviruses: Genome structure, replication, and pathogenesis. J. Med. Virol. 2020, 92, 418–423, Correction in J. Med. Virol. 2020, 92, 2249. [] [ CrossRef] [ PubMed] WHO. Six Years After COVID-19’s Global Alarm: Is the World Better Prepared for the Next Pandemic? Available online: https://www.who.int/ (accessed on 17 April 2026). Sithole, M.N.; Khan, M.R.; Mohammed, H.A.; Khan, R.A.; Naik, K.; Choonara, Y.E. A systematic review on vaccine developmental approaches: Evaluating efficacy, and addressing challenges of infectious diseases in the post-COVID-19 era. Virus Res. 2026, 367, 199720. [] [ CrossRef] [ PubMed] Cortese, P.; Amato, F.; Davino, A.; De Franchis, R.; Esposito, S.; Zollo, I.; Di Domenico, M.; Solito, E.; Zarrilli, F.; Gentile, L.; et al. The Immune Response to SARS-CoV-2 Vaccine in a Cohort of Family Pediatricians from Southern Italy. Cells 2023, 12, 1447. [] [ CrossRef] [ PubMed] Brüssow, H. Antivirals Targeting Coronavirus RNA-Dependent RNA Polymerase and Main Protease: From Mechanisms of Action to Outcomes in COVID-19 Clinical Trials. Microb. Biotechnol. 2026, 19, e70342. [] [ CrossRef] [ PubMed] Carabelli, A.M.; Peacock, T.P.; Thorne, L.G.; Harvey, W.T.; Hughes, J.; COVID-19 Genomics UK Consortium; Peacock, S.J.; Barclay, W.S.; de Silva, T.I.; Towers, G.J.; et al. SARS-CoV-2 variant biology: Immune escape, transmission and fitness. Nat. Rev. Microbiol. 2023, 21, 162–177. [] [ CrossRef] [ PubMed] Blanco-Melo, D.; Nilsson-Payant, B.E.; Liu, W.-C.; Uhl, S.; Hoagland, D.; Møller, R.; Jordan, T.X.; Oishi, K.; Panis, M.; Sachs, D.; et al. Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19. Cell 2020, 181, 1036–1045. [] [ CrossRef] [ PubMed] Hadjadj, J.; Yatim, N.; Barnabei, L.; Corneau, A.; Boussier, J.; Smith, N.; Péré, H.; Charbit, B.; Bondet, V.; Chenevier-Gobeaux, C.; et al. Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients. Science 2020, 369, 718–724. [] [ CrossRef] [ PubMed] Merad, M.; Martin, J.C. Pathological inflammation in patients with COVID-19: A key role for monocytes and macrophages. Nat. Rev. Immunol. 2020, 20, 355–362, Correction in Nat. Rev. Immunol. 2020, 20, 448. [] [ CrossRef] [ PubMed] Lucas, C.; Wong, P.; Klein, J.; Castro, T.B.R.; Silva, J.; Sundaram, M.; Ellingson, M.K.; Mao, T.; Oh, J.E.; Israelow, B.; et al. Longitudinal analyses reveal immunological misfiring in severe COVID-19. Nature 2020, 584, 463–469. [] [ CrossRef] [ PubMed] Lan, J.; Ge, J.; Yu, J.; Shan, S.; Zhou, H.; Fan, S.; Zhang, Q.; Shi, X.; Wang, Q.; Zhang, L.; et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature 2020, 581, 215–220. [] [ CrossRef] [ PubMed] Siddiqi, H.K.; Weber, B.; Zhou, G.; Regan, J.; Fajnzylber, J.; Coxen, K.; Corry, H.; Yu, X.G.; DiCarli, M.; Li, J.Z.; et al. Increased Prevalence of Myocardial Injury in Patients with SARS-CoV-2 Viremia. Am. J. Med. 2021, 134, 542–546. [] [ CrossRef] [ PubMed] Ferro, M.D.; Bussani, R.; Paldino, A.; Nuzzi, V.; Collesi, C.; Zentilin, L.; Schneider, E.; Correa, R.; Silvestri, F.; Zacchigna, S.; et al. SARS-CoV-2, myocardial injury and inflammation: Insights from a large clinical and autopsy study. Clin. Res. Cardiol. 2021, 110, 1822–1831, Correction in Clin. Res. Cardiol. 2021, 110, 1694. [] [ CrossRef] [ PubMed] Varga, Z.; Flammer, A.J.; Steiger, P.; Haberecker, M.; Andermatt, R.; Zinkernagel, A.S.; Mehra, M.R.; Schuepbach, R.A.; Ruschitzka, F.; Moch, H. Endothelial cell infection and endotheliitis in COVID-19. Lancet 2020, 395, 1417–1418. [] [ CrossRef] [ PubMed] Gelzo, M.; Cacciapuoti, S.; Pinchera, B.; De Rosa, A.; Cernera, G.; Scialò, F.; Comegna, M.; Mormile, M.; Gallicchio, A.; Fabbrocini, G.; et al. A Transient Increase in the Serum ANCAs in Patients with SARS-CoV-2 Infection: A Signal of Subclinical Vasculitis or an Epiphenomenon with No Clinical Manifestations? A Pilot Study. Viruses 2021, 13, 1718. [] [ CrossRef] [ PubMed] Ricci, D.; Demangel, C. From Bacterial Toxin to Therapeutic Agent: The Unexpected Fate of Mycolactone. Toxins 2023, 15, 369. [] [ CrossRef] [ PubMed] Gelzo, M.; Castaldo, A.; Giannattasio, A.; Scalia, G.; Raia, M.; Esposito, M.V.; Maglione, M.; Muzzica, S.; D’Anna, C.; Grieco, M.; et al. MIS-C: A COVID-19-associated condition between hypoimmunity and hyperimmunity. Front. Immunol. 2022, 13, 985433. [] [ CrossRef] [ PubMed] Serhan, C.N. Pro-resolving lipid mediators are leads for resolution physiology. Nature 2014, 510, 92–101. [] [ CrossRef] [ PubMed] Recalcati, S. Cutaneous manifestations in COVID-19: A first perspective. J. Eur. Acad. Dermatol. Venereol. 2020, 34, e212–e213. [] [ CrossRef] [ PubMed] McGonagle, D.; O’Donnell, J.S.; Sharif, K.; Emery, P.; Bridgewood, C. Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia. Lancet Rheumatol. 2020, 2, e437–e445. [] [ CrossRef] [ PubMed] Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.
