ReviewFrontiers in veterinary science2026
Mitochondria-associated endoplasmic reticulum membranes in canine and feline diabetic kidney disease: mechanistic links and nutritional implications.
Review in Frontiers in veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic kidney disease in dogs and cats is clinically relevant but mechanistically underdefined, and the dietary management of diabetic pets is still dominated by empirical control of glycemia, body weight, and renal nutrient load. Mitochondria-associated endoplasmic reticulum membranes (MAMs) are dynamic contact domains that coordinate calcium transfer, lipid exchange, ER stress, mitochondrial quality control, inflammatory signaling, and cell death. This review first summarizes the veterinary clinical context of canine and feline diabetic kidney disease, including proteinuria, microalbuminuria, hypertension, chronic kidney disease, and species-specific differences in diabetes pathophysiology. It then integrates MAM biology into core renal injury modules involving structural tethering proteins, the IP3R-GRP75-VDAC-MCU/MICU1 calcium axis, lipid metabolic enzymes, PERK/GRP78-mediated ER stress, mPTP opening, mitophagy, and inflammatory amplification. Because direct MAM evidence in diabetic dogs and cats remains limited, the MAM-related pathways discussed here are presented as hypotheses inferred from rodent DKD models, human cell lines, and broader metabolic-disease studies rather than as confirmed mechanisms in companion animals. Finally, we discuss how MAM-centered mechanisms may guide the development of functional prescription diets incorporating EPA/DHA, medium-chain triglycerides, L-carnitine, taurine, magnesium, N-acetylcysteine, antioxidants, resveratrol, and selected plant extracts, provided that efficacy and safety are validated using species-specific renal endpoints. This perspective may support a transition from empirical formulation to mechanism-informed precision nutrition for diabetic dogs and cats.
Indexed as
Identifiers
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.