ReviewInternational journal of molecular sciences2023
Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Association of CBC‑derived inflammation indices with prevalent CKD: a cross‑sectional analysis of a Chinese data set and NHANES.Annals of medicine · 2026Article
- An Integrated Therapeutic Strategy for Cardiorenal Syndrome to Target Oxidative Stress, Inflammation, and Fibrosis.Reviews in cardiovascular medicine · 2026Review
- Decoding cardiorenal crosstalk: Intercellular communication mechanisms and therapeutic insights in cardiorenal syndrome.iScience · 2026Review
- The Role and Therapeutic Potential of the STING Signaling Pathway in the Pathogenesis of Diabetic Nephropathy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Small molecules targeting regulated cell death for chronic kidney disease therapy.Journal of pharmaceutical analysis · 2026Review
- Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies.Biomolecules · 2026Review
- A Comprehensive Review on the Cardioprotective and Nephroprotective Effects of Semaglutide, and Its Therapeutic Efficacy and Mechanisms in Cardiorenal Syndrome.Drug design, development and therapy · 2026Review
- Connection Between Mitochondria and Rheumatoid Arthritis and Osteoarthritis: Personalized Treatment Strategies.Current pharmaceutical design · 2026Review
- Mitochondrial DNA efflux as a potential amplifier of systemic inflammatory network rewiring in heart failure with preserved ejection fraction.Frontiers in immunology · 2026Review
- Chronic cardiorenal syndrome: cardio-renal protective effect of SGLT2i.Renal failure · 2025Review
- Review
- Early Administration of N-Acetylcysteine Provides Renal and Cardiac Mitochondrial and Redox Protection, Preventing the Development of Cardio-Renal Syndrome Type IV Induced by 5/6NX.Antioxidants (Basel, Switzerland) · 2025Article
- Unveiling the Role of CCL3: A Driver of CIPN in Colon Cancer Patients?Biomedicines · 2025Review
- Cardiorenal Syndrome: Molecular Pathways Linking Cardiovascular Dysfunction and Chronic Kidney Disease Progression.International journal of molecular sciences · 2025Review
- Mitochondria-derived vesicles: A promising and potential target for tumour therapy.Clinical and translational medicine · 2025Review
- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
- Review of research progress in sepsis-associated acute kidney injury.Frontiers in molecular biosciences · 2025Review
- Cancerous Conditions Accelerate the Aging of Skeletal Muscle via Mitochondrial DNA Damage.International journal of molecular sciences · 2024Article
- When ASFV Infection Meets the cGAS-STING Signaling Pathway.Transboundary and emerging diseases · 2024Review
- Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease.Frontiers in cell and developmental biology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiorenal syndrome type 4 (CRS type 4) occurs when chronic kidney disease (CKD) leads to cardiovascular damage, resulting in high morbidity and mortality rates. Mitochondria, vital organelles responsible for essential cellular functions, can become dysfunctional in CKD. This dysfunction can trigger inflammatory responses in distant organs by releasing Damage-associated molecular patterns (DAMPs). These DAMPs are recognized by immune receptors within cells, including Toll-like receptors (TLR) like TLR2, TLR4, and TLR9, the nucleotide-binding domain, leucine-rich-containing family pyrin domain-containing-3 (NLRP3) inflammasome, and the cyclic guanosine monophosphate (cGMP)-adenosine monophosphate (AMP) synthase (cGAS)-stimulator of interferon genes (cGAS-STING) pathway. Activation of these immune receptors leads to the increased expression of cytokines and chemokines. Excessive chemokine stimulation results in the recruitment of inflammatory cells into tissues, causing chronic damage. Experimental studies have demonstrated that chemokines are upregulated in the heart during CKD, contributing to CRS type 4. Conversely, chemokine inhibitors have been shown to reduce chronic inflammation and prevent cardiorenal impairment. However, the molecular connection between mitochondrial DAMPs and inflammatory pathways responsible for chemokine overactivation in CRS type 4 has not been explored. In this review, we delve into mechanistic insights and discuss how various mitochondrial DAMPs released by the kidney during CKD can activate TLRs, NLRP3, and cGAS-STING immune pathways in the heart. This activation leads to the upregulation of chemokines, ultimately culminating in the establishment of CRS type 4. Furthermore, we propose using chemokine inhibitors as potential strategies for preventing CRS type 4.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.