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TsM_000695200.1

TsM_000695200.1

Overview

TsM_000695200.1 is a protein-associated biomedical target identifier used in research contexts involving sodium-glucose cotransporter 2 (SGLT2) inhibitors. In the publication contexts provided, it is discussed in relation to the SGLT2 pathway and to therapeutic agents such as empagliflozin and dapagliflozin, which are established SGLT2 inhibitors used in type 2 diabetes and increasingly studied in cardiovascular disease, heart failure, and chronic renal insufficiency/chronic kidney disease.

Biologically, the SGLT2 target is central to renal glucose handling and is therefore relevant to glucose-lowering therapy. The recent studies linked to this entity extend beyond glycemic control and examine broader effects of SGLT2 inhibition, including potential impacts on kidney outcomes, cardiovascular risk, appetite and body weight, cognitive dysfunction, oxidative stress, inflammation, and glycomic changes. In this context, TsM_000695200.1 is best understood as a target connected to the pharmacology of SGLT2 inhibitors rather than as a standalone clinically characterized protein with a widely established independent disease annotation.

Focus of Latest Publications

Recent publications have examined TsM_000695200.1 in the context of sodium glucose cotransporter-2 (SGLT2) inhibitor research, most often with dapagliflozin or related agents as the therapeutic intervention. Across these studies, the protein was investigated as a target in preclinical and clinical settings spanning cerebral ischemia-reperfusion injury, heart failure with ischemic cause, type 2 diabetes, metabolic dysfunction–associated steatotic liver disease, chronic kidney disease risk, appetite and body weight regulation, and cognitive dysfunction. Collectively, the literature reflects growing interest in SGLT2-related pathways beyond glucose lowering, including cardiovascular, renal, neurologic, and metabolic effects.

Several studies focused on dapagliflozin specifically. In a rat model of focal cerebral ischemia-reperfusion injury, dapagliflozin pretreatment was evaluated for prophylactic neuroprotection. Another experimental study assessed the effects of dapagliflozin on plasma N-glycome profiles in obese mice, comparing morning versus nighttime administration and finding time-of-day-dependent glycan changes, with nighttime dosing normalizing several high-fat-diet-induced alterations despite limited effects on blood glucose or body weight. In a separate in silico and in vivo study of diabetic cognitive dysfunction, dapagliflozin and empagliflozin were examined for interactions with targets including SGLT1/2, acetylcholinesterase, superoxide dismutase, receptor for advanced glycation end-products, and Interleukin 1 beta; both drugs improved behavioral and biochemical measures in diabetic rats, with dapagliflozin showing weaker docking interactions than empagliflozin for some AD-relevant targets.

Other publications placed TsM_000695200.1 within broader clinical and translational evaluations of SGLT2 inhibitors. One study investigated baseline ketone body metabolism as a predictor of SGLT2 inhibitor response in heart failure with ischemic cause across diverse genetic backgrounds, using metabolomics integration with population data. Another compared dapagliflozin and dulaglutide in patients with type 2 diabetes and metabolic dysfunction–associated steatotic liver disease, focusing on blood pressure and coronary flow. Additional work emulated target trials to compare individual SGLT2 inhibitors for cardiovascular outcomes in type 2 diabetes with moderate cardiovascular risk, and another nationwide emulated target trial in Taiwan assessed incident chronic kidney disease, cardiovascular events, and mortality among SGLT2 inhibitor users versus non-users in type 2 diabetes without preexisting CKD.

The recent literature also includes a review highlighting the persistent underuse of SGLT2 inhibitors in primary care despite guideline-supported roles in cardiovascular disease, chronic kidney disease, and heart failure. Another study examined appetite, food craving, and body weight in patients with type 2 diabetes and diabetic rat models, reporting limited impact of SGLT2 inhibitors on these outcomes. Overall, these publications position TsM_000695200.1 within an expanding body of work on SGLT2 inhibitor biology, with reported effects spanning neuroprotection, glycomic remodeling, cardiometabolic outcomes, renal protection, and cognitive function.

Key Publications

  • NEWJun Dapagliflozin pretreatment attenuates focal cerebral ischemia-reperfusion injury in rats. (Molecular biology reports, 2026, PMID 42334656): "This study evaluated the prophylactic neuroprotective effects of dapagliflozin (Dapa), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, in a non-diabetic rat model of cerebral ischemia/reperfusion (C/IR) injury."
  • NEWJun Ketone Body Metabolism and Sodium Glucose Cotransporter 2 Inhibitor Response in Heart Failure With Ischemic Cause: A Precision Medicine Approach Using Metabolomics Integration With Global Burden of Disease Population Data Across Diverse Genetic Backgrounds. (Journal of the American Heart Association, 2026, PMID 42261991): "SGLT2 (sodium glucose cotransporter 2) inhibitors demonstrate cardiovascular benefits, but interindividual response variability remains poorly understood."
  • Apr Effects of dapagliflozin and dulaglutide on blood pressure and coronary flow in liver steatosis patients with type 2 diabetes. (Journal of hypertension, 2026, PMID 42201656): "To investigate the effects of glucagon-like peptide-1 receptor agonists (GLP-1RAs) and sodium-glucose cotransporter-2 inhibitors (SGLT-2i) on cardiovascular function and hepatic metabolism in patients with type 2 diabetes mellitus (T2DM) and metabolic-dysfunction associated steatotic liver disease (MASLD)."
  • May Comparative Effectiveness of Individual Sodium Glucose Transporter 2 Inhibitors on Cardiovascular Outcomes in Type 2 Diabetes With Moderate Cardiovascular Risk: Emulation of a Target Trial. (Journal of the American Heart Association, 2026, PMID 42132163): "SGLT2 (sodium-glucose cotransporter 2) inhibitors reduce major adverse cardiovascular events (MACE) in type 2 diabetes."
  • May The SGLT2 inhibitor gap: why are we missing opportunities in primary care? (The British journal of general practice : the journal of the Royal College of General Practitioners, 2026, PMID 42134923): "Sodium-glucose cotransporter-2 (SGLT2) inhibitors have evolved from glucose-lowering agents to cornerstone therapies for cardiovascular disease (CVD), chronic kidney disease (CKD), and heart failure (HF)."
  • May Limited Impact of Sodium-Glucose Cotransporter-2 Inhibitors on Appetite and Body Weight: Evidence From Clinical and Rodent Studies. (Journal of Korean medical science, 2026, PMID 42117145): "This study investigated the effects of SGLT2 inhibitors on appetite, food craving, and body weight in patients with type 2 diabetes and diabetic rat models."
  • Jun SGLT2 inhibitors and the risk of incident chronic kidney disease in type 2 diabetes: a nationwide emulated target trial in Taiwan. (Diabetes research and clinical practice, 2026, PMID 42002149): "To compare the risk of incident chronic kidney disease (CKD), cardiovascular events, and mortality between users of sodium-glucose cotransporter 2 (SGLT2) inhibitors and non-users in patients with type 2 diabetes (T2D) without preexisting CKD."
  • May Time-of-Day Differences in the Plasma N-Glycome of Normal and Obese Mice and the Effects of Dapagliflozin Administered in the Morning or at Night. (Journal of proteome research, 2026, PMID 41948954): "with or without treatment using the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Dap), administered either in the morning or at night."
  • May Empagliflozin and dapagliflozin, sodium glucose cotransporter 2 inhibitors, may improve cognitive dysfunctions: in silico and in vivo findings. (Behavioural brain research, 2026, PMID 41819428): "...evaluating their in silico interactions with targets associated with oxidative stress, inflammation, and neuroprotection, including SGLT1, SGLT2, acetylcholinesterase (AChE), superoxide dismutase (SOD), receptor for advance glycation end-products (RAGE), and interleukin (IL)-1β."
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