bims-mimcat 2026-07-19 papers

Issue of 2026–07–19
six papers selected by
Sriparna Das, Visva Bharati University

Adv Exp Med Biol. 2026 ;1501 575-600

Metabolic Control of Immunity-Unveiling Neutrophil Mechanisms.

Bruna F Correia, Daniela Grosa, M Guadalupe Cabral.

Immune metabolism is a central determinant of neutrophil development, plasticity, and function. Once considered strictly glycolytic, neutrophils are now recognized as metabolically flexible cells that dynamically engage glycolysis, the pentose phosphate pathway (PPP), amino acid metabolism, and lipid oxidation to meet energetic and biosynthetic demands. Neutrophil metabolism is tightly regulated by nutrient-sensing and stress-response pathways, including mTOR, AMPK, and HIF-1α, which integrate environmental cues such as hypoxia and nutrient deprivation. In disease, metabolic rewiring underlies functional dysregulation, highlighting its role in chronic inflammatory disorders, metabolic syndromes, infection, and cancer. Therefore, targeting neutrophil metabolism offers therapeutic potential by restoring homeostasis, reducing inflammation, or enhancing antimicrobial and anti-tumor responses. Altogether, understanding neutrophil metabolic plasticity provides critical insights into immune regulation in health and disease, and offers promising avenues for novel therapies in chronic inflammation, metabolic disorders, infection, and cancer.

Keywords: Immunometabolism; Inflammation; Metabolic reprogramming; Neutrophil metabolism; Tumor microenvironment

DOI: https://doi.org/10.1007/978-3-032-12166-0_21

Adv Exp Med Biol. 2026 ;1501 165-189

Metabolic Symbiosis Between Cancer Cells and Endothelial Cells: A Key Driver of Tumor Angiogenesis.

Jacinta Serpa.

This chapter explores the critical role of angiogenesis in cancer, focusing on the metabolic processes involved in angiogenesis, particularly the metabolic remodeling of endothelial cells (ECs) and the symbiosis between cancer cells and ECs, which drive vascular development. Key topics include the influence of hypoxia and oxidative stress, and the reliance on different metabolic sources on EC function, as well as how various pro-angiogenic factors contribute to tumor vascularization. The importance of metabolic flexibility in ECs and its implications for cancer treatment will also be highlighted.

Keywords: Angiogenesis; Cancer cells; Endothelial cells (ECs); Metabolic remodeling; Metabolic symbiosis; Tumor microenvironment

DOI: https://doi.org/10.1007/978-3-032-12166-0_6

Adv Exp Med Biol. 2026 ;1501 303-323

Influence of RNA Modifications on Cancer Metabolism: Interplay with Hypoxia and Therapeutic Implications.

Catarina Guimarães-Teixeira, Vera Miranda-Gonçalves, Rui Henrique, Carmen Jerónimo.

Metabolic reprogramming is a well-established hallmark of cancer, with tumors often altering glucose and lipid metabolism to fuel their rapid growth and survival. Hypoxia, a common feature of the tumor microenvironment, exacerbates these metabolic shifts by the stabilization of hypoxia-inducible factors (HIFs), which drive the Warburg effect, enhancing tumor aggressiveness. Recent research has unveiled a critical link between hypoxia and epitranscriptomic modifications, particularly m6A methylation, which further influences cancer metabolism and progression. This review explores the complex relationship between hypoxia-induced epitranscriptomic alterations and cancer metabolic reprogramming, focusing on m6A RNA methylation. By exploring how these mechanisms interact to regulate glucose and lipid metabolism, we highlight potential therapeutic targets that could be exploited to disrupt the metabolic dependencies of tumors and improve treatment outcomes for hypoxia-induced malignancies.

Keywords: Cancer metabolism; Epitranscriptomics; Hypoxia; Metabolism crosslink; m6A; m6A immunity

DOI: https://doi.org/10.1007/978-3-032-12166-0_11

J Cardiovasc Transl Res. 2026 Jul 13. pii: 90. [Epub ahead of print]19(1):

Mitochondrial ncRNAs: From Pathological Regulation to Targeted Therapy in Cardiovascular Diseases.

Cheng Li, Qiong Yuan.

Heart failure (HF) is closely linked to mitochondrial dysfunction, featured by abnormal energy metabolism, excessive reactive oxygen species (ROS), and imbalanced mitochondrial dynamics. Clinically, effective targeted therapies for mitochondrial dysfunction are still lacking, which aggravates HF and multi-organ injury. Mitochondrial non-coding RNAs (mt-ncRNAs) form a regulatory network critical for mitochondrial function. Among them, mitochondrial-encoded circular RNAs (mecciRNAs) and mitochondrial double-stranded RNAs (mt-dsRNAs) are research hotspots. mecciRNAs protect the heart by assisting protein import and regulating mitochondrial pores and ROS; their degradation worsens HF, while exogenous supplementation alleviates injury. mt-dsRNAs arise from aberrant mitochondrial transcription and contribute to myocardial injury and remodeling via MAVS, cGAS-STING, and PNPT1 pathways. Gene therapy targeting mecciRNAs and mt-dsRNAs combined with mitochondrial delivery represents a promising strategy for HF treatment.

Keywords: Heart failure; Mitochondrial genome; Mitochondrial-penetrating peptides; Mt-dsRNA; Mt-mitochondrial-encoded circular RNAs

DOI: https://doi.org/10.1007/s12265-026-10809-0

Cancers (Basel). 2026 Jul 03. pii: 2150. [Epub ahead of print]18(13):

Myeloid-Derived Suppressor Cells in Cancer: Metabolic Reprogramming, Immune Crosstalk, and Therapeutic Targeting.

Andrea Sabatini, Maria Rita Assenza, Maria Teresa Bilotta, Paola Vacca, Nicola Tumino.

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of immature myeloid cells that accumulate in cancer and represent one of the major drivers of tumor-associated immunosuppression. MDSCs actively contribute to tumor progression by inhibiting both innate and adaptive immune responses, promoting angiogenesis, metastatic dissemination, and resistance to immunotherapy. Two major subsets have been identified, polymorphonuclear (PMN-) and monocytic (Mo-) MDSCs, each characterized by distinct phenotypic, metabolic, and suppressive properties. Within the tumor microenvironment (TME), MDSCs establish a complex network of interactions with T-, B-, NK-cells, dendritic cells, and macrophages, thereby orchestrating immune escape and tumor persistence. Recent evidence highlights the pivotal role of metabolic rewiring in regulating MDSC survival and suppressive activity. Enhanced aerobic glycolysis, fatty acid oxidation, amino acid depletion, reactive oxygen species (ROS) production, and adenosine metabolism collectively sustain MDSC-mediated immune dysfunction and shape the immunosuppressive TME. In particular, the crosstalk between PMN-MDSCs and NK cells has emerged as a critical mechanism of tumor immune evasion, leading to impaired NK cell cytotoxicity, altered activating receptor expression, and defective cytokine production. In this review, we summarize the current knowledge on the phenotypic and functional heterogeneity of MDSCs, their metabolic adaptations, and their interactions with immune effector populations in cancer. Furthermore, we discuss emerging therapeutic strategies aimed at targeting MDSC recruitment, differentiation, metabolic pathways, and suppressive functions. Understanding the molecular and metabolic mechanisms governing MDSC biology may provide novel opportunities to overcome tumor-induced immunosuppression and improve the efficacy of current cancer immunotherapies.

Keywords: TME; cancer; cancer therapy; immune crosstalk; metabolism; myeloid-derived suppressor cells

DOI: https://doi.org/10.3390/cancers18132150

Cell Chem Biol. 2026 Jul 16. pii: S2451-9456(26)00233-3. [Epub ahead of print]33(7): 966-981

The pyruvate dehydrogenase complex at the crossroads of cancer metabolism and cell death.

Xiutao Cai, Fangquan Chen, Ruirui Liang, Hu Tang, Qile Zhou, Junhao Lin, Rui Kang, Daolin Tang, Jiao Liu.

The pyruvate dehydrogenase complex (PDHC) is a key metabolic hub that couples glycolysis-derived carbon flux to the tricarboxylic acid cycle and mitochondrial function. Its activity is regulated by pyruvate dehydrogenase kinases, phosphatases, and lysine acylation, enabling dynamic responses to metabolic and stress signals. In cancer, dysregulation of the PDK-PDHC axis reduces PDH flux, promotes aerobic glycolysis, and enhances adaptation to mitochondrial and oxidative stress, thereby influencing susceptibility to regulated cell death. Recent studies further suggest that PDHC exhibits considerable structural and functional plasticity under hypoxia and redox stress. Growing preclinical and translational evidence indicates that targeting the PDK-PDHC axis may redirect metabolic flux and improve therapeutic responses in selected tumor contexts. This review summarizes current understanding of PDHC regulation, its context-dependent roles in regulated cell death, and the therapeutic potential and challenges of exploiting PDH-related metabolic vulnerabilities in cancer.

DOI: https://doi.org/10.1016/j.chembiol.2026.06.009