Immunometabolic Dysfunction
Immunometabolic Dysfunction - Related Videos
11:12
Immunometabolic Circuits in Infection for Advancing Host Directed Therapies
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Cited by 1 •
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Here, a protocol for designing, constructing, and delivering tetracycline-controlled based inducible synthetic circuit is presented. The effect of the synthetic circuits on parasite elimination and cytokine expression can be studied by channelizing the presented pipeline. This protocol is relevant for researchers studying synthetic circuit-based therapeutics in infectious diseases.
06:26
Mouse Model of Metabolic Dysfunction-Associated Steatotic Liver Disease with Fibrosis
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Cited by 1 •
2025
Mouse model of metabolic dysfunction-associated steatotic liver disease (MASLD) with metabolic dysfunction, hepatic gene expression changes, and liver histopathological alterations that resemble human MASLD, including fibrosis that progresses to advanced fibrosis stage 3. This model can be used in studies of MASLD pathophysiology and in pre-clinical studies of new therapies.
09:39
Mapping Dysfunctional Protein-Protein Interactions in Disease
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2025
Here, we present a protocol to enable the capture and identification of disease-specific protein-protein interactions from native cells and tissues using chemical probes and mass spectrometry. The resulting interaction datasets are analyzed through a dedicated web-based platform to reveal dynamic network dysfunctions and pathway alterations linked to disease.
06:38
Early Detection of Drug-Induced Renal Hemodynamic Dysfunction Using Sonographic Technology in Rats
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Cited by 14 •
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Early stage hemodynamic dysfunction is critical to the development of kidney disease. Yet, detection methodologies are limited. Recent advances in sonography provide a noninvasive, accurate option for early detection of kidney injury. This study outlines a step-by-step, sonographic methodology for detecting kidney dysfunction using a drug-induced nephrotoxicity rat model.
12:03
Fertility Preservation in Patients with Severe Ovarian Dysfunction
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Cited by 3 •
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We present details of laboratory procedures for drug-free in vitro activation (IVA) of ovarian follicles for patients with severe ovarian dysfunction. This method could increase the number of retrievable oocytes per ovarian hyperstimulation and benefit fertility preservation for those patients.
FAQs
A key mechanism is reciprocal feedback: activated immune cells change their use of glucose and lipids, alter mitochondrial activity, and modify cytokine production. Those metabolic changes can influence immune signaling in return, so the relationship is not one-directional. This feedback helps explain why disturbed energy handling may sustain inflammatory activity rather than remaining a separate metabolic problem.
Persistent stress, infection, or nutrient excess can push this feedback system away from coordination. Under these conditions, immune-cell metabolic changes and altered cytokine production occur alongside impaired insulin signaling. The significance is cumulative: metabolic regulation can worsen immune activation, while inflammatory activity can further disrupt how cells respond to insulin.
Glucose and lipid use, mitochondrial activity, and cytokine production represent connected control points rather than isolated markers. A shift in one can accompany changes in the others as immune cells respond to ongoing stress. Examining these components together gives a more complete picture of whether inflammation and energy regulation are coordinated or becoming mutually reinforcing.
The two-way nature of immunometabolic dysfunction matters because it can connect local immune activity with broader metabolic consequences. When inflammatory signaling and impaired insulin signaling reinforce each other, a disturbance may contribute to a wider disease pattern rather than remaining confined to one pathway. This provides a mechanistic link among immune, metabolic, and clinical research.
In medicine, this framework is relevant to obesity, diabetes, cardiovascular disease, cancer, and chronic inflammatory disorders. Its value is not that every condition has an identical mechanism, but that each can be examined through interactions among inflammation, cellular fuel use, mitochondrial activity, cytokines, and insulin signaling. That perspective supports cross-disease investigation.
Research focused on biomarkers aims to identify measurable features of disrupted immune-metabolic communication. The overview points to glucose and lipid use, mitochondrial activity, cytokine production, and insulin signaling as informative pathway areas. Assessing such features could help characterize disease-associated imbalance and track whether an intervention reduces harmful inflammation while improving metabolic coordination.
Therapeutic strategies in this area are directed toward restoring metabolic balance while reducing harmful inflammation, rather than treating either process in isolation. The rationale follows from the feedback mechanism: changing metabolic regulation may influence immune activity, and reducing inflammatory disruption may support insulin signaling. This combined goal is relevant when both systems are involved in disease.