Evidence map›Paper›PMID 37606388›Full record

ReviewPathophysiology : the official journal of the International Society for Pathophysiology2023

Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications.

Alyssa Williams, Rosi Bissinger, Hala Shamaa, Shivani Patel, Lavern Bourne, Ferruh Artunc, Syed M Qadri

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pathophysiology : the official journal of the International Society for Pathophysiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
10.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Alyssa WilliamsFaculty of Science, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.
Rosi BissingerDivision of Endocrinology, Diabetology and Nephrology, Department of Internal Medicine, University Hospital Tübingen, 72076 Tübingen, Germany.
Hala ShamaaFaculty of Health Sciences, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.ORCID 0009-0001-1032-3562
Shivani PatelFaculty of Health Sciences, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.
Lavern BourneFaculty of Health Sciences, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.
Ferruh ArtuncDivision of Endocrinology, Diabetology and Nephrology, Department of Internal Medicine, University Hospital Tübingen, 72076 Tübingen, Germany.
Syed M QadriFaculty of Health Sciences, Ontario Tech University, Oshawa, ON L1G 0C5, Canada.ORCID 0000-0002-2193-932X
Ontario Tech University · CAUniversity Children's Hospital Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes Mellitus (DM) is a complex metabolic disorder associated with multiple microvascular complications leading to nephropathy, retinopathy, and neuropathy. Mounting evidence suggests that red blood cell (RBC) alterations are both a cause and consequence of disturbances related to DM-associated complications. Importantly, a significant proportion of DM patients develop varying degrees of anemia of confounding etiology, leading to increased morbidity. In chronic hyperglycemia, RBCs display morphological, enzymatic, and biophysical changes, which in turn prime them for swift phagocytic clearance from circulation. A multitude of endogenous factors, such as oxidative and dicarbonyl stress, uremic toxins, extracellular hypertonicity, sorbitol accumulation, and deranged nitric oxide metabolism, have been implicated in pathological RBC changes in DM. This review collates clinical laboratory findings of changes in hematology indices in DM patients and discusses recent reports on the putative mechanisms underpinning shortened RBC survival and disturbed cell membrane architecture within the diabetic milieu. Specifically, RBC cell death signaling, RBC metabolism, procoagulant RBC phenotype, RBC-triggered endothelial cell dysfunction, and changes in RBC deformability and aggregation in the context of DM are discussed. Understanding the mechanisms of RBC alterations in DM provides valuable insights into the clinical significance of the crosstalk between RBCs and microangiopathy in DM.

Indexed as

anemiacell deathcomplicationsdeformabilitydiabetesmetabolismmicrocirculationred blood cellsthrombosis

Identifiers

PMID37606388
PMCPMC10443300
OpenAlexW4385490962

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.