Hypoxia-inducible factor 1α (HIF-1α) protein has been identified as an aggressive malignant phenotype marker for numerous tumors; therefore, the detection of HIF-1α has become increasingly significant.
In this work, we developed a type of magnetically induced self-assembled electrochemical aptamer nanobiosensor for detecting HIF-1α protein. This nanobiosensor utilized the magnetism of hydrothermal-calcination-synthesized α-ferric oxide/ferriferrous oxide (α-Fe
2
O
3
/Fe
3
O
4
, αFO/FFO) magnetic heterogeneous nanorods (MHNRs) to realize magnetically induced self-assembly; further, gold nanoparticles (AuNPs) were used to reinforce the electron transfer capacity and realize secure immobilization of the aptamer via Au–S bonds. Finally, we adopted cyclic voltammetry (CV), electrochemical impedance spectroscopy (EIS), and differential pulse voltammetry (DPV) for the electrochemical characterization, condition optimization, and performance analysis of the nanobiosensor, respectively.
The nanobiosensor revealed a favorable linear relation in the range of 0.1–1,000 ng/mL with a variance R
2
of 0.995 and limit of detection of 0.112 ng/mL, excellent sensitivity, faithful reproducibility with a relative standard deviation (RSD) of 2.28%, reliable 13-d stability with an RSD of 1.71%, and accredited detection capacity for real samples with recoveries of 97.71%–107.47% and RSDs ≤ 3.47%.
In this study, we developed a magnetically induced self-assembled electrochemical aptamer nanobiosensor for ultrasensitive detection of HIF-1α protein. The nanosensor delivers outstanding analytical performance with a facile assay strategy suitable for point-of-care testing, suggesting its promising prospects for clinical tests.
Xiangjun Zhou, Hezhong Ouyang, Li-Ping Sui et al.· Frontiers in Chemistry· 0 citations
Mesenchymal stem cells (MSCs) and regulatory T cells (Tregs) form a key immunoregulatory axis essential for maintaining immune homeostasis and treating autoimmune diseases, transplant rejection, and inflammatory disorders. Although both MSCs and Tregs have been individually studied, a clear synthesis of how MSCs regulate Treg function across distinct mechanistic layers and disease contexts remains lacking. MSCs regulate Treg differentiation, expansion, and functional stability through paracrine signaling, intercellular contact–dependent pathways, extracellular vesicle (EV)–mediated transfer of microRNAs (miRNAs) and proteins, mitochondrial transfer, and metabolic and epigenetic reprogramming. These mechanisms restore Th17/Treg balance, suppress inflammation, and promote tissue repair. Preclinical studies demonstrate strong therapeutic potential in multiple immune–mediated diseases; however, clinical translation remains limited. Unlike previous studies, this review integrates soluble and exosomal signaling pathways, compares shared and disease‐specific regulatory mechanisms, and critically evaluates MSC source variability, methodological limitations, and causes of clinical inconsistency. It aims to provide a conceptual framework to guide future mechanistic studies and clinical development of MSC–Treg–based therapies.